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    What 2012 atopy risk protective factor What 2012 atopy risk protective factor Presentation Transcript

    • WHAT YOU SHOULD HAVE READ BUT….2012  atopy risk & protective factorsAttilio BonerUniversity ofVerona, Italy
    • • Prevalence and time trends
    • Prenatal negative life events increases cord blood IgE:interactions with dust mite allergen and maternal atopy. Peters, Allergy 2012;67:545Background: Prenatal exposure to both stress & aeroallergens(dust mite) may modulate the fetal immune system. These exposuresmay interact to affect the newborn immune response. We examinedassociations between prenatal maternal stress & cord blood total IgEin 403 predominately low-income minority infants enrolledin the Asthma Coalition on Community, Environment and Social Stress(ACCESS) project. We also examined potential modifying effectsof maternal atopy and maternal dust mite exposure.
    • Prenatal negative life events increases cord blood IgE:interactions with dust mite allergen and maternal atopy. Peters, Allergy 2012;67:545 1) Overall the negative domains score was The Crisis in Family positively associated Systems survey with increased was administered cord blood IgE. to mothers prenatally. 2) Cord blood IgE levels Negative life event increased 0.10 IU/ml domain score was derived. for each unit increase Dust mite allergen in dust in the number of negative from pregnant mothers„ domains reported bedrooms. by the mother.
    • Prenatal negative life events increases cord blood IgE:interactions with dust mite allergen and maternal atopy. Peters, Allergy 2012;67:545 Relationship for atopic mothers between log cord blood IgE & n°of domains with negative life events by high vs low dust mite allergen. The Crisis in Family Systems survey was administered to mothers prenatally. Negative life event domain score was derived. Dust mite allergen in dust from pregnant mothers„ bedrooms.
    • Prenatal negative life events increases cord blood IgE:interactions with dust mite allergen and maternal atopy. Peters, Allergy 2012;67:545 Relationship for atopic mothers between log cord blood IgE & n°of domains with negative life events by high vs low dust mite allergen. Among children The Crisis in Family of atopic Systems survey mothers, the positive was administered association between to mothers prenatally. stress & IgE Negative stronger was life event domain high dust mite in the score was derived. group. Dust mite allergen in dust from pregnant mothers„ bedrooms.
    • Prenatal negative life events increases cord blood IgE:interactions with dust mite allergen and maternal atopy. Peters, Allergy 2012;67:545 Relationship for nonatopic mothers between log cord blood IgE & n°of domains with negative life events by high vs low dust mite allergen. The Crisis in Family Systems survey was administered to mothers prenatally. Negative life event domain score was derived. Dust mite allergen in dust from pregnant mothers„ bedrooms.
    • Prenatal negative life events increases cord blood IgE:interactions with dust mite allergen and maternal atopy. Peters, Allergy 2012;67:545 Relationship for nonatopic mothers between log cord blood IgE & n°of domains with negative life events by high vs low dust mite allergen. In children Themothers without of Crisis in Family Systems survey a history of atopy, was administered the positive to mothers prenatally. association between Negative & IgE was stress life event most evident domain score was derived. in the low allergen Dust mite allergen in dust group. from pregnant mothers„ bedrooms.
    • Prenatal negative life events increases cord blood IgE:interactions with dust mite allergen and maternal atopy. Peters, Allergy 2012;67:5451) These data suggest that prenatal maternal stress may influence fetal immune system development in children born to mothers both with and without a history of atopy.2) Moreover, the demonstration of synergistic effects of stress & aeroallergen exposure points to the need for a multi pronged intervention approach to reducing disease risk.
    • Resilience in low-socioeconomic-status children with asthma: adaptations to stress. Chen, JACI 2011;128:970Background:Low socioeconomic status (SES) is a strong predictor of manyhealth problems, including asthma impairment;however, little is understood about why some patients defy this trendby exhibiting good asthma control despite living in adverseenvironments.Objective:This study sought to test whether a psychological characteristic,the shift-and-persist strategy (dealing with stressors by reframingthem more positively while at the same time persisting in optimisticthoughts about the future), protects low-SES children with asthma.
    • Resilience in low-socioeconomic-status children with asthma: adaptations to stress. Chen, JACI 2011;128:970 121 children aged 9 to 18 yrs with asthma. 1) „„I thought about the Shift-and-persist scores. things I was learning The tendency to shift oneself from the situation or in response to stressors about something good was measured by using the that would come from it‟‟. Cognitive Restructuring scale of the Responses to Stress questionnaire. 2) „„I always feel good about Smith, J Consult Clin Psychol 2000;68:976. my future‟‟. Higher scores indicated a higher tendency to positively reappraise stressful situations.
    • Resilience in low-socioeconomic-status children with asthma: adaptations to stress. Chen, JACI 2011;128:970 121 children aged 9 to 18 yrs with asthma. Children who came from Shift-and-persist scores. low-SES backgrounds The tendency to shift oneself but who engaged in in response to stressors shift-and-persist strategies was measured by using the displayed less asthma Cognitive Restructuring scale inflammation at baseline of the Responses to Stress questionnaire. (p <0.05) Smith, J Consult Clin Psychol 2000;68:976. as well as less asthma impairment Higher scores indicated a higher (p <0.01) tendency to positively reappraise stressful situations. at the 6-mo period.
    • Resilience in low-socioeconomic-status children with asthma: adaptations to stress. Chen, JACI 2011;128:970 121 children aged 9 to 18 yrs with asthma. Children In contrast, Shift-and-persist scores. who came from shift-and-persist low-SES backgrounds The tendency to shift oneself but who engaged in strategies in response to stressors shift-and-persist strategies were not beneficial was measured by using the displayed less asthma Cognitive Restructuring scale among high-SES of the Responses to Stress inflammation at baseline children with questionnaire. (p <0.05) as well as asthma. Smith, J Consult Clin Psychol 2000;68:976. less asthma impairment Higher scores indicated a higher (p <0.01) tendency to positively reappraise stressful situations. at the 6-mo period.
    • Allergy is associated with suicide completion with apossible mediating role of mood disorder-a population- based study Qin, Allergy 2011;66:658 % subjects with a history of hospital contact for allergy 2 – 27 096 completedsuicides.467 571 live controls. 1 – 1.17 % 0.79 % 0 Suicide Controls
    • Allergy is associated with suicide completion with apossible mediating role of mood disorder-a population- based study Qin, Allergy 2011;66:658 % subjects with a history of hospital contact for allergy 2 – We observed a 27nonsignificantly 096 completed stronger effectsuicides. in women than in men and a467 571 live controls. 1 – 1.17 % stronger effect 0.79 % for individuals at high ages 0 Suicide Controls
    • Allergy is associated with suicide completion with apossible mediating role of mood disorder-a population- based study Qin, Allergy 2011;66:658 OR for suicide 2 – 27 096 completedsuicides. 1.59467 571 live controls. 1 – 0 Allergy that led to inpatient treatment
    • Allergy is associated with suicide completion with apossible mediating role of mood disorder-a population- based study Qin, Allergy 2011;66:658 OR for suicide Allergy increased 2 – suicide risk only in 27 persons with no 096 completedsuicides. history of mood 1.59 disorder, whereas467 571eliminated it live controls. 1 – suicide risk in those with a history of mood disorder. 0 Allergy that led to inpatient treatment
    • Impaired type I and III interferon response to rhinovirus infection during pregnancy and asthma Forbes, Thorax 2012;67:209Background:• Acute respiratory tract infections are common ailments to all individuals and the human rhinoviruses (HRVs) cause most of these infections.• Pregnant women have increased susceptibility and disease severity to viral infections like influenza and HRVs, as do asthmatics.• Successful pregnancy requires immunological modulation to permit fetal tolerance.
    • Impaired type I and III interferon response to rhinovirus infection during pregnancy and asthma Forbes, Thorax 2012;67:209 A) Pregnant women had significantly reduced 1) 10 stable pregnant asthmatics; innate IFN responses 2) 10 stable not pregnant asthmatics; to HRV infection 3) 10 pregnant non-asthmatic women; (p<0.02), persistin 4) 10 who were ≥6 mo post partum; g ≥6 mo 5) 10 who were not pregnant. post partum (p≤0.02). Peripheral blood mononuclear cells (PBMCs) cultured with B) Pregnant asthmatics HRV43 and HRV1B. had significantly reduced IFNλ responses IFNα and IFNλ (lambda) compared with from culture supernatants. healthy non-pregnant women (p≤0.034).
    • Impaired type I and III interferon response to rhinovirus infection during pregnancy and asthma Forbes, Thorax 2012;67:209 Interferon-α (IFNα) and IFNλ responsesof peripheral blood mononuclear cells (PBMCs) from pregnant women to in vitro human rhinovirus (HRV) stimulation. Isolated PBMCs from pregnant (P), postpartum (PP) and non-pregnant healthy control (HC) women were stimulated with HRV43 or HRV1B. = IFNα = IFNλ
    • Impaired type I and III interferon response to rhinovirus infection during pregnancy and asthma Forbes, Thorax 2012;67:209 Interferon-α (IFNα) and IFNλ responsesof peripheral blood mononuclear cells (PBMCs) from asthmatic women to in vitro human rhinovirus (HRV) stimulation. Isolated PBMCs from non-pregnant healthy control (HC) women and asthmatics who were pregnant (PA) and not pregnant (A) were stimulated = IFNα = IFNλ with HRV43 or HRV1B.
    • Impaired type I and III interferon response to rhinovirus infection during pregnancy and asthma Forbes, Thorax 2012;67:209 Interferon-α (IFNα) and IFNλ responses Reduced antiviral IFNsof peripheral blood mononuclear asthma provide an asthmatic women during pregnancy and cells (PBMCs) from important to in vitro human rhinovirus (HRV) stimulation. mechanism for increased susceptibility, morbidity and mortality in pregnant women with respiratory viral infection. Isolated PBMCs from non-pregnant healthy control (HC) women and asthmatics who were pregnant (PA) and not pregnant (A) were stimulated = IFNα = IFNλ with HRV43 or HRV1B.
    • Febrile respiratory illnesses in infancy and atopy are risk factors for persistent asthma and wheeze Kusel, Eur Respir J 2012;39:876 At age of 10 years % of children 60 - 147 children at 60% 50 – high atopic risk. 40 – Followed from birth to age 10 yrs. 30 – Respiratory infections 20 – 26% collected prospectively 20.4% and viral aetiology 18% 10 – ascertained. 000 Current Current Persistent Atopy wheeze and Atopic doctor-diagnosed eczema asthma wheeze eczema and asthma.
    • Febrile respiratory illnesses in infancy and atopy are risk factors for persistent asthma and wheeze Kusel, Eur Respir J 2012;39:876 At age of 10 years % of children 60 - 147 children at 60% 50 – high atopic risk. 35.8% experienced 40 – Followed from lower at least one birth to age 10 yrs.respiratory infection 30 – (LRI) associated Respiratory infections with fever and/or 20 – 26% collected prospectively 20.4% wheeze in first and viral aetiology 18% 10 – ascertained. life. year of 000 Current Current Persistent Atopy wheeze and Atopic doctor-diagnosed eczema asthma wheeze eczema and asthma.
    • Febrile respiratory illnesses in infancy and atopy are risk factors for persistent asthma and wheeze Kusel, Eur Respir J 2012;39:876 In children who had wheezy or febrile LRI in infancy and were atopic by 2 yrs 147 children at RR at age 10yrs for high atopic risk. 5 - 4.92 Followed from birth 4 - p<0.001 to age 10 yrs. 3 – 3.51 Respiratory infections p<0.001 collected prospectively and viral aetiology 2 – ascertained. 1 – Atopy wheeze and doctor-diagnosed eczema and asthma. 0 persistent current wheeze asthma
    • Febrile respiratory illnesses in infancy and atopy are risk factors for persistent asthma and wheeze Kusel, Eur Respir J 2012;39:8761. Severe viral respiratory infections in infancy and early atopy are risk factors for persistent wheeze and asthma.2. The strongest marker of the asthmatogenic potential of early life infections was concurrent fever.3. The occurrence of fever during respiratory illnesses is an important marker of risk for wheeze and asthma later in childhood, suggesting it should be measured in prospective studies of asthma aetiology.
    • Staphylococcal-derived superantigen enhances peanut induced Th2 responses in the skin. Forbes-Blom, Clin Exp Allergy 2012;42:305 Concomitant exposure to Peanut extract (PE) staphylococcal-derived superantigenTh2 model Th2 response in the skin draining lymph nodes
    • Staphylococcal-derived superantigen enhances peanut induced Th2 responses in the skin. Forbes-Blom, Clin Exp Allergy 2012;42:305 Concomitant exposure to Peanut extract (PE) staphylococcal-derived superantigen Significantly enhanced specific Th2 responses.Th2 model (+) Th2 response in the skin draining lymph nodes
    • Staphylococcal-derived superantigen enhances peanut induced Th2 responses in the skin. Forbes-Blom, Clin Exp Allergy 2012;42:305Exposure of staphylococcal enterotoxin B (SEB) when being primed to peanut extract (PE) leads to an enhanced PE-dependent CD4 Th2 response.c (a) (b) Absolute n° (a) and proportion (b) of CD4+ GFP+ T cells present in the draining auricular lymph node 24h after final intradermal boost.
    • Staphylococcal enterotoxin B compromises the immune tolerant status in the airway mucosa. Liu T, Clin Exp Allergy 2012;42:3751) Staphylococcal enterotoxin B (SEB) is an enterotoxin produced by the bacterium Staphylococcus aureus. SEB may contaminate ingested food and induce gastrointestinal dysfunction. SEB interferes with the function of the immune system in the airway mucosa, such as to be involved in the pathogenesis of airway allergy.2) Integrin alphavbeta6 (avb6) is produced by epithelial cells in response to external stimuli, such as wound and inflammation. Our recent study data also show that intestinal epithelial cells express detectable avb6 that has protelytic activity and can convert the precursor of transforming growth factor (TGF)β into the active form of TGFβ. TGFβ plays a critical role in the Treg development. Tolergenic DCs (TolDC) express TGFβ and aldehyde dehydrogenase (ALDH) that can induce CD4+ CD25- T cells to Foxp3+ Tregs.
    • Staphylococcal enterotoxin B compromises the immune tolerant status in the airway mucosa. Liu T, Clin Exp Allergy 2012;42:3751) Staphylococcal enterotoxin B (SEB) is an enterotoxin produced by the bacterium Staphylococcus aureus. SEB may contaminate ingested food and induce gastrointestinal dysfunction. in avb6 The increases in SEB and decreases SEB interferes with the function of the immune system in the airway mucosa, such as to be involvedassociated in nasal epithelium are in the pathogenesis of airway allergy. compromises of immune tolerance with the in the nasal mucosa.2) Integrin alphavbeta6 (avb6) is produced by epithelial cells in response SEB has stimuli,ability wound and inflammation. to external the such as to suppress Our recent study data also show that intestinal epithelial cells express detectable avb6 that has protelyticavb6 and can convert the expression of activity in nasal epithelial cells. the precursor of transforming growth factor (TGF)β into the active form of TGFβ. TGFβ plays a critical role in the Treg development. Tolergenic DCs (TolDC) express TGFβ and aldehyde dehydrogenase (ALDH) that can induce CD4+ CD25- T cells to Foxp3+ Tregs.
    • Staphylococcal enterotoxin B compromises the immune tolerant status in the airway mucosa. Liu T, Clin Exp Allergy 2012;42:375 Avb6 expression is suppressed in the allergic rhinitis (AR) nasal epithelium• The immune tolerant components, tolerogenic dendritic cells (TolDC) P<0.01 & regulatory T cells (Treg), were assessed in the surgically removed nasal mucosa from patients with allergic rhinitis (AR) Staphylococcal enterotoxin B (SEB) or non-AR chronic rhinitis. levels are increased in the allergic rhinitis nasal epithelium.• Contents of Staphylococcal enterotoxin B & integrin alphavbeta6 P<0.01 (avb6) in the nasal epithelium assessed using enzyme-linked immunoassay.
    • Staphylococcal enterotoxin B compromises the immune tolerant status in the airway mucosa. Liu T, Clin Exp Allergy 2012;42:375 Avb6 expression is suppressed in the allergic rhinitis (AR) nasal epithelium• The immune tolerant components, tolerogenic dendritic cells (TolDC) The components P<0.01 & regulatory T cells (Treg), were of immune tolerance assessed in the surgically removed machinery, nasal mucosa from patients with allergic rhinitisTregs TolDCs & (AR) Staphylococcal enterotoxin B (SEB) or non-AR chronic rhinitis. were suppressed levels are increased in the allergic rhinitis nasal epithelium. in the AR• Contents of Staphylococcal enterotoxin B &mucosa. nasal integrin alphavbeta6 P<0.01 (avb6) in the nasal epithelium assessed using enzyme-linked immunoassay.
    • Gram+ bacteria on grass pollen exhibit adjuvant activity inducing inflammatory T cell responses Heydenreich, Clin Exp Allergy 2012;42:76 Background Recently, it has been established that pollen grains contain Th2-enhancing activities besides allergens. Objective The aim of this study was to analyse whether pollen carry additional adjuvant factors like microbes and what immunological effects they may exert.
    • Gram+ bacteria on grass pollen exhibit adjuvant activity inducing inflammatory T cell responses Heydenreich, Clin Exp Allergy 2012;42:76 A complex mixture of bacteria and moulds was detected on grass pollen: Timothy pollen grains collected and disseminated - Gram-negative that are known on agar plates. to favour Th1-directed immune responses. Immunologic effects of microbial products - Gram positive bacteria e.g on DC & T cell responses. Bacillus cereus & Bacillus subtilis. - Moulds.
    • Gram+ bacteria on grass pollen exhibit adjuvant activity inducing inflammatory T cell responses Heydenreich, Clin Exp Allergy 2012;42:76 Supernatants of homogenized Gram+ bacteria induce CD80, CD83 expression in immature dendritic cells. Timothy pollen grains collected and disseminated on agar plates. Immunologic effects of microbial products on DC & T cell responses.
    • Gram+ bacteria on grass pollen exhibit adjuvant activity inducing inflammatory T cell responses Heydenreich, Clin Exp Allergy 2012;42:76 Supernatants of homogenized Gram+ Contact of immature bacteria induce CD80, CD83 expression in dendritic cells (DC) immature dendritic cells. from grass pollen allergic Timothy pollensupernatants donors with grains collected homogenized of and disseminated on Gram-positive bacteria agar plates. induced maturation of DC Immunologic effects as measured of microbial products by up-regulation of CD80 on DC & T cell responses. and CD83.
    • Gram+ bacteria on grass pollen exhibit adjuvant activity inducing inflammatory T cell responses Heydenreich, Clin Exp Allergy 2012;42:76 Induction of proinflammatory cytokines in immature dendritic cells. Timothy pollen grains collected and disseminated on agar plates. Immunologic effects of microbial products on DC & T cell responses.
    • Gram+ bacteria on grass pollen exhibit adjuvant activity inducing inflammatory T cell responses Heydenreich, Clin Exp Allergy 2012;42:76Conclusions and Clinical Relevance These data indicatethat grass pollen is colonized by several microorganismsthat influence the immune response differently.Similar to LPS, supernatants of homogenizedGram-positive bacteria may serve as adjuvantsby augmenting DC maturation and inflammatory Th1, Th2and Th17 responses helping to initiate allergicimmune responses.
    • Innate lymphoid cells responding to IL-33 mediate airway hyperreactivity independently of adaptive immunity Kim JACI 2012;129:216BackgroundAsthma has been considered an immunologic diseasemediated by TH2 cells and adaptive immunity.However, clinical and experimental observationssuggest that additional pathways might regulateasthma, particularly in its nonallergic forms,such as asthma associated with air pollution,stress, obesity, and infection.ObjectivesOur goal was to understand TH2 cell–independent conditions that mightlead to airway hyperreactivity (AHR), a cardinal feature of asthma.
    • Innate lymphoid cells responding to IL-33 mediate airway hyperreactivity independently of adaptive immunity Kim JACI 2012;129:216 Glycolipid antigens directly induced alveolar macrophages1) Activate natural killer T (NKT) cells. to produce IL-33, as well as IL-13.2) Airway hyperreactivity developed rapidly
    • Innate lymphoid cells responding to IL-33 mediate airway hyperreactivity independently of adaptive immunity Kim JACI 2012;129:216 Glycolipid antigens directly induced Because plant pollens, house dust, andalveolar macrophages some bacteria1) Activate natural killer T (NKT) cells. activate NKT cells, contain glycolipids that can directly to produce IL-33, these studies suggest that as well as IL-13. AHR and asthma can fully develop or be greatly enhanced2) Airway hyperreactivity developed rapidly through innate immune mechanisms.
    • Innate lymphoid cells responding to IL-33 mediate airway hyperreactivity independently of adaptive immunity Kim JACI 2012;129:216 Schematic of the IL-33–ST2 axis in the development of AHR. On activation by glycolipid antigens, NKT cells induce macrophages, DCs, and type II pneumocytes toproduce IL-33, which in turnactivates natural helper andNKT cells to produce IL-13,resulting in the development of AHR.IL-33 can also activate mast cells, eosinophils, and basophils. ST2 = IL-33R = IL-33 Receptor
    • Gestational age at birth and risk of allergic rhinitis in young adulthood. Crump JACI 2011;127:1173 For subjects born extremely preterm (23-28 weeks) OR for 630,090 infants born in Sweden including 27,953 1.0 – born preterm (<37 wks). Prescription of nasal 0.5 – 0.70 corticosteroids and oral 0.45 antihistamines 0.0 Nasal corticosteroid Both nasal age, 25.5-37.0 yrs. prescription corticosteroid and oral antihistamine prescription
    • Gestational age at birth and risk of allergic rhinitis in young adulthood. Crump JACI 2011;127:1173 These findings suggest that low gestational age For subjects born extremely at birth independent preterm (23-28 weeks) OR for 630,090 infants born in of fetal growth is Sweden including 27,953 1.0 – associated with a born preterm (<37 wks). decreased risk of Prescription of nasal young allergic rhinitis in 0.5 – 0.70 corticosteroids and oral adulthood, possibly 0.45 antihistaminesa protective because of 0.0 Nasal corticosteroid Both nasal effect of earlier age, 25.5-37.0 yrs. prescription corticosteroid and exposure to pathogens. oral antihistamine prescription
    • Infant antibiotic use and wheeze and asthma risk: a systematic review and meta-analysis Penders ERJ 2011;38:295 OR for 2 – wheeze/asthma 18 longitudinal studies. Effect of antibiotic use on wheeze/ asthma. 1 – 1.27 Early antibiotic use
    • Infant antibiotic use and wheeze and asthma risk: a systematic review and meta-analysis Penders ERJ 2011;38:295 When we eliminated OR for studies with possible 2 – wheeze/asthma reverse causation 18 longitudinal studies. and respiratory tract infections leading Effect of antibiotic use to antibiotic use, on wheeze/ asthma. the pooled risk estimate 1 – 1.27 was attenuated to OR 1.12. Early antibiotic use
    • Prenatal or Early-Life Exposure to Antibiotics and Risk of Childhood Asthma: A Systematic Review Murk Pediatrics 2011;127:1125 OR for asthma if exposed to Studies published 3 – antibiotic in the first yr of life between 1950 and July 1, 2010, that assessed associations 2 – between antibiotic 2.04 exposure during 1.52 1.25 pregnancy or in the 1 – first year of life and asthma at ages 0 to 18 yrs. 0 all studies retrospective prospective studies studies
    • Prenatal or Early-Life Exposure to Antibiotics and Risk of Childhood Asthma: A Systematic Review Murk Pediatrics 2011;127:1125 OR for asthma if exposed to Studies published 3 – antibiotic in the first yr of life between 1950 and Risk estimate July 1, 2010, that assessed studies for associations 2 – between adjusted that antibiotic 2.04 for respiratory exposure during 1.52 1.25 pregnancy or in the infections is 1 – first year 1.16 OR of life and asthma at ages 0 to 18 yrs. 0 all studies retrospective prospective studies studies
    • Prenatal or Early-Life Exposure to Antibiotics and Risk of Childhood Asthma: A Systematic Review Murk Pediatrics 2011;127:1125 OR for asthma if exposed to Studies published to Antibiotics seem 3 – antibiotic in the first yr of life between 1950 and slightly increase July 1, 2010, that the risk of assessed associations childhood asthma. 2 – between antibiotic Reverse causality and 2.04 exposure during protopathic bias seem 1.52 1.25 pregnancy possible to be or in the 1 – first year of life confounders for and asthma at this relationship. ages 0 to 18 yrs. 0 all studies retrospective prospective studies studies
    • •paracetamol
    • The Association of Acetaminophen and Asthma Prevalence and Severity McBride Pediatrics 2011;128:1181• The epidemiologic association between acetaminophen use and asthma prevalence and severity in children and adults is well established.• A variety of observations suggest that acetaminophen use has contributed to the recent increase in asthma prevalence in children: 1) the strength of the association; 2) the consistency of the association across age, geography, and culture; 3) the dose-response relationship; 4) the timing of increased acetaminophen use and the asthma epidemic;
    • The Association of Acetaminophen and Asthma Prevalence and Severity McBride Pediatrics 2011;128:1181• The epidemiologic association between acetaminophen use and asthma prevalence and severity in children and adults is well established.• A variety of observations suggest that acetaminophen use has contributed to the recent increase in asthma prevalence in children: 5) the relationship between per-capita sales of acetaminophen and asthma prevalence across countries; 6) the results of a double-blind trial of ibuprofen and acetaminophen for treatment of fever in asthmatic children; 7) the biologically plausible mechanism of glutathione depletion in airway mucosa.
    • The Association of Acetaminophen and Asthma Prevalence and Severity McBride Pediatrics 2011;128:1181• The epidemiologic association between acetaminophen use and Until future studies document the safety asthma prevalence and severity in children and adults is well of this drug, children with asthma or at established. risk for asthma should avoid the use of• A variety of observations suggest that acetaminophen use has acetaminophen. contributed to the recent increase in asthma prevalence in children: 5) the relationship between per-capita sales of acetaminophen and asthma prevalence across countries; 6) the results of a double-blind trial of ibuprofen and acetaminophen for treatment of fever in asthmatic children; 7) the biologically plausible mechanism of glutathione depletion in airway mucosa.
    • •Allergens
    • Correlation of specific IgE to shrimp with cockroachand dust mite exposure and sensitization in an inner-city population Wang JACI 2011;128:834 Shrimp specific IgE levels were correlated with exposure to cockroach but only among children with positive IgE levels to cockroach. 504 serum samples. sIgE to shrimp, cockroach (Blattella germanica) and Dermatophagoides farinae.
    • Correlation of specific IgE to shrimp with cockroachand dust mite exposure and sensitization in an inner-city population Wang JACI 2011;128:834 Shrimp specific IgE levels were correlated with exposure to cockroach but only among children with positive IgE levels to cockroach. High exposure to 504 serum samples. B. Germanica in sIgEtheshrimp, was to home cockroach significantly (Blattella germanica) andcorrelated with Dermatophagoides IgE higher shrimp farinae. levels.
    • Correlation of specific IgE to shrimp with cockroachand dust mite exposure and sensitization in an inner-city population Wang JACI 2011;128:834 Shrimp specific IgE levels were correlated with exposure to cockroach but only among children with positive IgE levels to cockroach. In contrast, 504 high exposure serum samples. sIgE to shrimpmite to dust , cockroach in the home (Blattella germanica) and was not correlated with Dermatophagoides farinae. IgE levels. shrimp
    • Correlation of specific IgE to shrimp with cockroachand dust mite exposure and sensitization in an inner-city population Wang JACI 2011;128:834Conclusions•For children with evidence of IgE-mediated sensitization tocockroach and shrimp, having high exposure to cockroach in thehome can contribute to higher shrimp IgE levels, which might notcorrelate with clinical reactivity.•Further patient evaluations with clinical historiesof shrimp exposure and reactions, as well as oral food challenges,would have to be performed to confirm these findings.
    • •Allergens •acari
    • Inhibition of house dust mite–induced allergic airwaysdisease by antagonism of microRNA-145 is comparable to glucocorticoid treatment. Collison JACI 2011;128:160  MicroRNAs (miRNAs) are important regulators of the immune system by promoting the catabolism of their target transcripts as well as attenuating their translation.  Blocking miRNA function may provide a new nonsteroidal anti-inflammatory approach to treatment.
    • Inhibition of house dust mite–induced allergic airwaysdisease by antagonism of microRNA-145 is comparable to glucocorticoid treatment. Collison JACI 2011;128:160 Sensitized and then aeroallergen- challenged with house dust mite Allergic airways disease, and alterations in the expression ofmiRNAs: miR-145, miR-21, and let-7b
    • Inhibition of house dust mite–induced allergic airwaysdisease by antagonism of microRNA-145 is comparable to glucocorticoid treatment. Collison JACI 2011;128:160 Sensitized and then aeroallergen- challenged with house dust mite Inhibition of miR-145, but not miR-21 or lethal-7b, inhibited eosinophilic inflammation, mucus hypersecretion, TH2 cytokine production, and airway hyperresponsiveness. Allergic airways disease, and alterations in the expression ofmiRNAs: miR-145, miR-21, and let-7b
    • Invariant NKT cells are required for airway inflammation induced by environmental antigens Wingender J Exp Med 2011;208:1151• Recent increases in the prevalence of asthma and other allergic diseases have prompted investigators to consider the role of the environment in the genesis of atopy.• We have previously reported that house dust extracts (HDEs) contain ligands that activate DCs by toll-like receptor 2 (TLR-2)-, TLR4-, and TRL9- dependent pathways. Boasen J JACI 2005;116:185-191. Batzer G Immunobiology 2007;212:491-498.• We have further established that HDEs have the potential to function as Th2 adjuvants in mice receiving intranasal (i.n.) OVA vaccinations. Ng N. JACI 2006;117:1074-1081. Lee S.M. AJRCMB 2011;44:341-349.
    • Invariant NKT cells are required for airway inflammation induced by environmental antigens Wingender J Exp Med 2011;208:1151• Novel invariant natural killer T cell-activating antigens found in house dust extracts.• Invariant natural killer T (iNKT) cells are effector cells activated by CD1d presentation of glycolipid antigens.• Until now, iNKT antigens have been found in 2 bacteria, one of which is the causative agent in Lyme disease.• We report the discovery of iNKT antigens in house dust extracts.
    • Invariant NKT cells are required for airway inflammation induced by environmental antigens Wingender J Exp Med 2011;208:1151• These experimental findings highlights the complexity of house dust as an immunostimulant.• More specifically, we provide direct evidence that living environments have the potential to activate iNKT cells through their T-cell receptor and potentially by other pathways, adding support to the view that iNKT cells have clinical relevance in human asthma and other diseases.
    • House dust mite extract downregulates C/EBPα* in asthmatic bronchial smooth muscle cells Miglino ERJ 2011;38:50 1. Increased IL-6 protein House dust mite and proliferation of BSM (HDM) extracts cells of asthma patients only. 2. HDM extract reduced the C/EBPα expression in BSM cells of asthma patients. 3. HDM extract elicited both protease-dependent Bronchial smooth muscle cells and –independent (BSM) responses.* enhancer-binding protein
    • House dust mite extract downregulates C/EBPα* in asthmatic bronchial smooth muscle cells Miglino ERJ 2011;38:50 1. Increased IL-6 protein House dust mite and proliferation of BSM HDM exposure (HDM) extracts cells of asthma patients contributes only. to inflammation and remodelling 2. HDM extract reduced the C/EBPα expression in BSM by a nonimmune cells of asthma patients. cell-mediated mechanism via a direct interaction 3. HDM extract elicited both protease-dependent with BSM cells. and –independent Bronchial smooth muscle cells (BSM) responses.* enhancer-binding protein
    • Playing a dirty trick on airway smooth muscle: house dust mite does it again Zuyderduyn ERJ 2011;38:4  Airway smooth muscle cells isolated from asthmatic proliferate faster in culture and produce more chemokines and an altered array of extracellular matrix proteins compared with those of healthy individuals.  The increase in ASM proliferation in asthma is thought to be associated with decreased levels of CCAAT enhancer protein (c/EBP)α (encoded by the CEBPA gene), a crucial controller of cell cycle progression, differentiation and inflammation.
    • Playing a dirty trick on airway smooth muscle: house dust mite does it again Zuyderduyn ERJ 2011;38:4  In addition to increased proliferation, interleukin (IL)-6 release (induced by growth factors) is increased in ASM from asthmatics.  House dust mite (HDM) exerts direct effects on various cell types, including protease-dependent cell detachment in epithelial cells and IgE-independent activation of mast cells.
    • Playing a dirty trick on airway smooth muscle: house dust mite does it again Zuyderduyn ERJ 2011;38:4  Exposure of rabbit ASM strips to the purified Der p 1 allergen increased airway hyperresponsiveness to acetylcholine and reduced relaxation responses to isoproterenol, and this effect was attributed to the protease activity of Der p 1.  These data suggest that the effects of HDM can be IgE-dependent and –independent, as well as protease-dependent and –independent.
    • Antibacterial antibody responses associated with thedevelopment of asthma in house dust mite-sensitised and non-sensitised children. Hales, Thorax 2012;67:321Background:Infants who develop house dust mite (HDM) allergyand HDM sensitised children with severe persistent asthma havelow antibody responses to the P6 antigen of Haemophilus influenzae.Objective:1) To measure the development of antibody to 2 ubiquitous bacteria of the respiratory mucosa in a prospective birth cohort at high risk of allergic disease.2) To assess which responses are associated with asthma and atopy.
    • Antibacterial antibody responses associated with thedevelopment of asthma in house dust mite-sensitised and non-sensitised children. Hales, Thorax 2012;67:321 Development of IgG1 antibody (ng/ml) IgG1 and IgG4 antibody to: - H. influenzae (P4, P6) - S. pneumoniae (PspA, PspC) surface antigens. Yearly blood samples * * ** * *** * * of children aged 1-5 yrs. Children were stratified based on: - HDM sensitisation - Asthma * ** at 5 yrs of age. *p<0.05, **p<0.01, ***p<0.001
    • Antibacterial antibody responses associated with thedevelopment of asthma in house dust mite-sensitised and non-sensitised children. Hales, Thorax 2012;67:321 Development of IgG1 antibody (ng/ml) IgG1 and IgG4 antibody to: - H. influenzae (P4, P6) HDM-sensitised children - S. pneumoniae (PspA, PspC) surface had lower antigens. IgG1 antibody titres to the blood samples Yearly bacterial antigens, * * ** * *** * * of and early responses children aged 1-5 yrs. (<3yrs and before Children were stratified based on:development the of HDM sensitisation - HDM sensitisation - Asthma asthma). and * ** at 5 yrs of age. *p<0.05, **p<0.01, ***p<0.001
    • Antibacterial antibody responses associated with thedevelopment of asthma in house dust mite-sensitised and non-sensitised children. Hales, Thorax 2012;67:321 Development of IgG1 antibody (ng/ml) IgG1 and IgG4 antibody to: - H. influenzae (P4, P6) - S. HDM-sensitisedPspC) pneumoniae (PspA, surface antigens. children have early defective Yearly blood samples * * ** * *** * * ofantibody responses children aged 1-5 yrs. to bacteria Children were stratified that are associated based on: - HDM sensitisation with asthma. - Asthma * ** at 5 yrs of age. *p<0.05, **p<0.01, ***p<0.001
    • Antibacterial antibody responses associated with thedevelopment of asthma in house dust mite-sensitised and non-sensitised children. Hales, Thorax 2012;67:321Possible explanations1. The low IgG antibody response could enhance atopy and asthma by increasing the susceptibility to bacterial infection and the exposure to pharmacologically active bacterial products.2. Underlying immune responses to the bacteria and allergens influence immune responses to each other when they are copresented at the mucosa to increase the degree of sensitisation.3. Altered antibody responses are just markers that show people with atopy and asthma have alterations in an aspect of their mucosal immune system that extends beyond the response to allergens.
    • Antibacterial antibody responses associated with thedevelopment of asthma in house dust mite-sensitised and non-sensitised children. Hales, Thorax 2012;67:321Possible explanations1. The low IgG antibody response could enhance atopy and asthma by increasing the susceptibility to bacterial infection Increased bacterial colonisation, and the exposure to pharmacologically active bacterial products. including both H influenzae and S pneumoniae,2. Underlying immune responses to the bacteria and allergens has been associated with susceptibility influence immune responses to each other when they are copresented at the mucosaasthma and degree of sensitisation. to to increase the wheezing attacks.3. Altered antibody responses are just markers that show people with atopy and asthma have alterations in an aspect of their mucosal immune system that extends beyond the response to allergens.
    • Protease-activated receptor 2-dependent fluid secretion from airway submucosal glands by house dust mite extract Cho JACI 2012;129:529BackgroundThe submucosal gland (SMG) is important in the control of airwaysurface fluid.Protease-activated receptor (PAR) 2 contributes to the pathophysiologyof allergies in response to nonspecific allergens bearing proteases andanion secretion.House dust mites (HDMs) have abundant proteases that can activatePAR2, but little is known about the direct effect of HDM on SMGsecretion.ObjectiveTo investigate the effect of HDMs on glandular secretion and itsmechanism in allergic patients, patients with chronic rhinosinusitis(CRS), or both.
    • Protease-activated receptor 2-dependent fluid secretion from airway submucosal glands by house dust mite extract Cho JACI 2012;129:529Inferior nasal 1) HDM induced a turbinates. significantly higher55 patients classified secretion rate into four groups: and number of 1. the control, 2. allergic rhinitis (AR), responding glands 3. chronic rhinosinusitis (CRS), in the AR and 4. AR + CRS. AR+CRS groupsMucus bubbles from than in the individual submucosal control group. gland (SMGs).
    • Protease-activated receptor 2-dependent fluid secretion from airway submucosal glands by house dust mite extract Cho JACI 2012;129:529Inferior nasal 2) Patients in the turbinates. CRS group, who had no55 patients classified HDM-specific IgE, into four groups: showed a 1. the control, higher response 2. allergic rhinitis (AR), than the control group, 3. chronic rhinosinusitis (CRS), and its response 4. AR + CRS. was suppressed byMucus bubbles from a PAR2-selective individual submucosal antagonist. gland (SMGs).
    • Protease-activated receptor 2-dependent fluid secretion from airway submucosal glands by house dust mite extract Cho JACI 2012;129:529 Quantitative measurement of glandular secretion.A. Harvest of nasal mucosa from the inferior nasal turbinate.B. Experimental setup.C. Mucus bubbles from glands under oil are visualized by using bright-field microscopy and side-light illumination.D. Example of mucus bubbles formed on the surface of nasal turbinates 30 minutes after stimulation.
    • Protease-activated receptor 2-dependent fluid secretion from airway submucosal glands by house dust mite extract Cho JACI 2012;129:529 Responses to HDM. Plots of averaged secretion rates versus time for each group.Inferior nasal *p < 0.05 turbinates.55 patients classified into four groups: 1. the control, 2. allergic rhinitis (AR), 3. chronic rhinosinusitis (CRS), 4. AR + CRS.Mucus bubbles from individual submucosal gland (SMGs).
    • Protease-activated receptor 2-dependent fluid secretion from airway submucosal glands by house dust mite extract Cho JACI 2012;129:529 Conclusions HDM allergens can induce glandular secretion in patients with AR, CRS, or both, and PAR2 represents a possible mechanism for nonspecific hyperreactivity in inflammatory airway diseases.
    • Gene-by-environment effect of house dust mite on purinergic receptor P2Y12 (P2RY12) & lung function in children with asthma. Bunyavanich, Clin Exp Allergy 2012;42:229Background Distinct receptors likely exist for leukotriene (LT)E4,a potent mediator of airway inflammation.Purinergic receptor P2Y12 is needed for LTE4-induced airwaysinflammation, and P2Y12 antagonism attenuates house dust miteinduced pulmonary eosinophilia in mice. Although experimental datasupport a role for P2Y12 in airway inflammation, its role in humanasthma has never been studied.Objective To test for association between variants in the P2Y12 gene(P2RY12) and lung function in human subjects with asthma,and to examine for gene-by-environment interaction with housedust mite exposure.
    • Gene-by-environment effect of house dust mite on purinergic receptor P2Y12 (P2RY12) & lung function in children with asthma. Bunyavanich, Clin Exp Allergy 2012;42:229Background Distinct receptors likely exist for leukotriene (LT)E4,a potent mediator of airway inflammation. House dust mitePurinergic receptor P2Y12 is needed for LTE4-induced airwaysinflammation, and P2Y12 antagonism attenuates house dust mite exposure causedinduced pulmonary eosinophilia in mice. Although experimental data significantsupport a role for P2Y12 in airway inflammation, its role in humanasthma has never been studied. gene-by-environmentObjective To test for association between variants in the P2Y12 gene(P2RY12) and lung functioneffects. in human subjects with asthma,and to examine for gene-by-environment interaction with housedust mite exposure.
    • Gene-by-environment effect of house dust mite on purinergic receptor P2Y12 (P2RY12) & lung function in children with asthma. Bunyavanich, Clin Exp Allergy 2012;42:229 •5 SNPs in P2RY12 were associated with multiple lung function measures 19 single nucleotide (P-values 0.006–0.025). polimorphisms (SNPs) •Haplotypes in P2RY12 were also associated with lung function in P2RY12. (P-values 0.0055–0.046). Children with asthma (n=422) •House dust mite exposure modulated associations between & their parents (n=1266) . P2RY12 and lung function, with minor allele homozygotes exposed to Associations between house dust mite demonstrating these SNPs & lung function. worse lung function than those unexposed (significant interaction P- House dust mite exposure. values 0.0028–0.040).
    • Gene-by-environment effect of house dust mite onpurinergic receptor P2Y12 (P2RY12) & lung function in children with asthma. Bunyavanich, Clin Exp Allergy 2012;42:229 Relationship between P2RY12 single nucleotide polymorphisms & airways responsiveness stratified by house dust mite exposure. (a) House dust mite exposure
    • •Allergens•Cane e gatto
    • The long-term protective effects of domestic animals in the home. Erwin CEA 2011;41:920 There is a critical age at which exposure to animals can have a protective effect. Specifically, animal exposure needs to occur in the first year of life. When tolerance to cats was first described, many authors assumed that it would be comparable with the effect of farm animals, which appears to be dependant on an early exposure to endotoxin or environmental microorganisms. But in many studies, measurements of endotoxin have not been higher in homes with domestic animals and the effect of cat ownership appears to be cat specific.
    • The long-term protective effects of domestic animals in the home. Erwin CEA 2011;41:920 Children living in a house with a cat can produce high levels of IgE to mite while remaining „tolerant‟ to the cat. Current estimates of high exposure to cat suggest that 20–50 times more allergen is inhaled as compared with mite allergen. A large part of the estimated 1 μg of cat allergen inhaled per day is swallowed. On this basis, daily exposure to cat, or dog, allergens is not far different from the doses used for sublingual „desensitization‟.
    • Lifetime dog and cat exposure and dog- and cat- specific sensitization at age 18 years Wegienka CEA 2011;41:979 Detroit Childhood OR for sensibilization Allergy Study birth to dog at age 18 yrs cohort contacted at 1.0 – the age 18 years. Sensitization to dog 0.5 – or cat defined as animal-specific 0.50 0.0 IgE ≥ 0.35 kU/L. Those with an indoor dog during the first year of life
    • Lifetime dog and cat exposure and dog- and cat- specific sensitization at age 18 years Wegienka CEA 2011;41:979 Detroit Childhood OR for sensibilization Allergy Study birth to cat at age 18 yrs cohort contacted at 1.0 – the age 18 years. Sensitization to dog 0.5 – or cat defined as animal-specific 0.52 0.0 IgE ≥ 0.35 kU/L. With an indoor cat in the first year of life
    • Lifetime dog and cat exposure and dog- and cat- specific sensitization at age 18 years Wegienka CEA 2011;41:979 Detroit Childhood life The first year of OR for sensibilization Allergy Study birth is the critical period to cat at age 18 yrs cohort contacted at during childhood when 1.0 – the age 18 years. to indoor exposure dogs or cats 0.5 – Sensitization to dog 0.52 influences or cat defined as to sensitization animal-specific these animals. 0.0 IgE0.35 kU/L. With an indoor cat in the first year of life
    • Risk factors for new-onset cat sensitization amongadults: A population-based international cohort study Olivieri JACI 2012;129:420BackgroundCat exposure during childhoodhas been shown to increase the risk ofdeveloping cat sensitization, while the effectofcat exposure in adulthood has not yet been established.ObjectiveTo evaluate new-onset sensitization to cat in adulthoodin relation to changes in cat keeping.
    • Risk factors for new-onset cat sensitization among adults: A population-based international cohort study Olivieri JACI 2012;129:420 % adults who became6292 European sensitized to cat 4.0 – Community Respiratory Health Survey I (ECRHS I) 3.5 – 3.0 – 3.7% participants 2.5 – (20 to 44 years). 2.0 –Reevaluated 1.5 – 9 years later. 1.0 –Serum IgE level 0.5 - ≥0.35 kU/L. 0.0
    • Risk factors for new-onset cat sensitization among adults: A population-based international cohort study Olivieri JACI 2012;129:4206292 European RR for new onset Community Respiratory cat sensitization Health Survey I 2.0 – (ECRHS I) participants 1.5 – 1.85 (20 to 44 years). 1.0 –Reevaluated 9 years later. 0.5 -Serum IgE level 0.0 Cat acquisition during follow-up when ≥0.35 kU/L. compared with those without a cat at both surveys.
    • Risk factors for new-onset cat sensitization amongadults: A population-based international cohort study Olivieri JACI 2012;129:420ConclusionAcquiring a cat in adulthood nearly doubles the riskof developing cat sensitization.Hence, cat avoidance should be considered in adults, especiallyin those sensitized to other allergens and reporting a historyof allergic diseases.
    • Effect of prenatal indoor pet exposure on the trajectory of total IgE levels in early childhood Havstad JACI 2011;128:880 Background The presence of pets in a home during the prenatal period and during early infancy has been associated with a lower prevalence of allergic sensitization and total IgE levels in middle childhood. No studies have examined the effect of pet exposure in a population-based cohort by using multiple early-life measures of serum total IgE. Objectives We sought to examine within-individual longitudinal trends in total IgE levels during early childhood and assess the effect of indoor prenatal pet exposure on those trends.
    • Effect of prenatal indoor pet exposure on the trajectory of total IgE levels in early childhood Havstad JACI 2011;128:880 Log-transformed IgE values by age. Birth cohort. 1187 infants. 1 to 4 measurements of total IgE collected from birth to 2 yrs of age.
    • Effect of prenatal indoor pet exposure on the trajectory of total IgE levels in early childhood Havstad JACI 2011;128:880 Log-transformed IgE values by age. The trajectory Birth cohort. of IgE levels was 1187 infants. nonlinear, with an 1 to 4 measurements of total accelerated IgE collected from birth to 2 yrs increase before of age. 6 months.
    • Effect of prenatal indoor pet exposure on the trajectory of total IgE levels in early childhood Havstad JACI 2011;128:880 Birth cohort. 1187 infants. 1 to 4 measurements of total IgE collected from birth to 2 yrs of age.
    • Effect of prenatal indoor pet exposure on the trajectory of total IgE levels in early childhood Havstad JACI 2011;128:880 Total IgE levels were lower across Birth entire early-life period the cohort. 1187 infants. there was when prenatal indoor 1 to 4 measurements of total pet exposure IgE collected from birth to 2 yrs of age. 0.001). (p<
    • Effect of prenatal indoor pet exposure on the trajectory of total IgE levels in early childhood Havstad JACI 2011;128:880 % reduction in total IgE due to pet exposure and type of delivery. 0 – Birth cohort. vaginal Cesarean 1187 infants. -10 – -16% section 1 to 4 measurements of total -20 – p<0.06 IgE collected from birth to 2 yrs of age. -30 – -40 - -43% p<0.001 -50 –
    • Effect of prenatal indoor pet exposure on the trajectory of total IgE levels in early childhood Havstad JACI 2011;128:880 % reduction in total IgE due to pet exposure and type of delivery. 0 – Birth cohort. vaginal Cesarean Pet exposure and 1187 infants. delivery mode -10 – -16% section 1 to 4 measurements of total -20 – p<0.06 might be markers IgE collected from birth to 2 yrs infant exposure of of age. -30 – to distinct microbes. -40 - -43% p<0.001 -50 –
    • High environmental relative moldiness index during infancy as a predictor of asthma at 7 years of age Reponen Ann Allergy Asthma Immunol 2011;107:120 % children asthmatic at the age 7 yrs 20 – A high-risk birth cohort from infancy to 7 years of age. 15 – 18% 10 – Mold assessed by a DNA-based analysis for 05 – the 36 molds. 00
    • High environmental relative moldiness index during infancy as a predictor of asthma at 7 years of age Reponen Ann Allergy Asthma Immunol 2011;107:120 aORs (95% CIs) for Asthma Diagnosis at 7 Years of Age by Predictor Variables of the 176 Study ChildrenAbbreviations: aOR, adjusted odds ratio; CI, confidence interval;ERMI, Environmental Relative Moldiness Index.These variables remained statistically significant (P <0.05) in a full multivariate model.
    • Asthma related to Alternaria sensitization: an analysis of skin-test and serum-specific IgE efficiency based on the bronchial provocation test Fernández CEA 2011;41:649 % pts with a (+) specific challenge 70 – 74 asthmatic 60 – patients sensitized to Alternaria . 50 – 61% 40 – Specific bronchial 30 – challenge with this 20 – mould. 10 – .0
    • Asthma related to Alternaria sensitization: an analysis of skin-test and serum-specific IgE efficiency based on the bronchial provocation test Fernández CEA 2011;41:649 % pts with a (+) specific Skin prick testing challenge almost perfectly 70 – 74 asthmatic outcome predicted the 60 – of bronchoprovocation patients sensitized to Alternaria . tests. 50 – 61% 40 – Weals around 5.5 mm Specific bronchial 90% in diameter had 30 – challenge with this a probability of 20 – mould. positive challenge. 10 – .0
    • Asthma related to Alternaria sensitization: an analysis of skin-test and serum-specific IgE efficiency based on the bronchial provocation test Fernández CEA 2011;41:649 % pts with a (+) specific A CAP value 70 – challenge 74 asthmatickUA/L ≥ 16 60 – predicted a positive patients sensitized tobronchial challenge Alternaria . 50 – 61% 40 – result with 99% Specific bronchial accuracy, 30 – challenge with this 20 – mould. 10 – .0
    • Meta-analysis of mould and dampness exposure on asthma and allergy in eight European birth cohorts: an ENRIECO initiative Tischer, Allergy 2011;66:1570 OR for early asthma symptoms 0,3 – 31 742 children from 8 ongoing European birth 0.2 – cohorts. Reported mould or 1.39 dampness exposure in 0.1 – early life. Development of allergic 0.0 – disorders in children. Exposure to visible mould and/or dampness during first 2 yrs of life
    • Meta-analysis of mould and dampness exposure on asthma and allergy in eight European birth cohorts: an ENRIECO initiative Tischer, Allergy 2011;66:1570 A moudly home OR for early asthma symptoms enviroment in early life 0,3 – is associated with an 31 742 children from 8 increased risk of ongoing European birth 0.2 – asthma particulary in cohorts. young children and Reported mould or allergic rhinitis 1.39 dampness exposure in symptoms in 0.1 – early life. school-age children Development of allergic 0.0 – disorders in children. Exposure to visible mould and/or dampness during first 2 yrs of life
    • Lung function decline in relation to mould and dampness in the home: the longitudinal European Community Respiratory Health Survey ECRHS II Norbäck Thorax 2011;66:396 % of houses with Participants in the 50 – European Respiratory 50.1% Health Survey initially examined aged 20-45 yrs 40 – 41.3% and 9 yrs later (n=6443). 30 – Dampness (water damage 20 – or damp spots) and indoor mould, ever and in 10 – the last 12 months. 0 Any dampness Indoor mould
    • Lung function decline in relation to mould and dampness in the home: the longitudinal European Community Respiratory Health Survey ECRHS II Norbäck Thorax 2011;66:396 Additional decline in FEV1 ml/year 0 Participants in the European Respiratory -2.25 Health Survey initially examined aged 20-45 yrs and 9 yrs later (n=6443). -5 Dampness (water damage -7.43 or damp spots) and indoor mould, ever and in the last 12 months. -10 Women with In women with dampness observed damp spots at home in the bedroom
    • Lung function decline in relation to mould and dampness in the home: the longitudinal European Community Respiratory Health Survey ECRHS II Norbäck Thorax 2011;66:396 Additional decline in FEV1 ml/year 0 Participants in the Dampness and Europeanmould growth indoor Respiratory -2.25 Health Survey initially is common in examined aged 20-45 yrs dwellings, and the andpresence of(n=6443). 9 yrs later damp -5 is a risk factor for Dampness (water damage lung function decline, -7.43 orespecially in women. damp spots) and indoor mould, ever and in the last 12 months. -10 Women with In women with dampness observed damp spots at home in the bedroom
    • Lung function decline in relation to mould and dampness in the home: the longitudinal European Community Respiratory Health Survey ECRHS II Norbäck Thorax 2011;66:3961) The additional mean lung function decline, -2.25 ml/year for self- reported dampness and -7.43 ml/year for observed dampness in the bedroom, is of the same order of magnitude as estimated for moderate tobacco smoking in the same ECRHS cohort.2) The reason for the sex difference in effect remains unclear, but could be due to either higher susceptibility or a longer exposure time in the dwelling for women.
    • •Smokingpassive-active
    • School absenteeism among children living with smokers Levy Pediatrics 2011;128:650 More days absent from school per years than children living with 0 smokers in the home. 2 – Health and absenteeism among school children aged 1 – 1.54 6 to 11 yrs. 1.06 0 1 ≥2 Adults who smoked in the home
    • School absenteeism among children living with smokers Levy Pediatrics 2011;128:650 Living with ≥2 adults who smoked in the home OR for 3 – Health and absenteeism among 2 – 2.65 school children aged 6 to 11 yrs. 1 – 1.77 00 ≥3 ear infections Having a chest in the previous 12 cold in the 2 months weeks before interview
    • School absenteeism among children living with smokers Levy Pediatrics 2011;128:650 Living with ≥2 adults who smoked in the home OR for 3 – Tobacco smoke Health and exposure has absenteeism among significant 2 – 2.65 school children aged consequences for 6children and families to 11 yrs. 1 – 1.77 above and beyond child morbidity, including academic disadvantage 00 and financial burden. ≥3 ear infections Having a chest in the previous 12 cold in the 2 months weeks before interview
    • Secondhand Smoke Exposure and Neurobehavioral Disorders Among Children in the United States Kabir, Pediatrics 2011;128:263 % children exposed to SHS in the home Children ≤12 yrs 7 – in the United States. 6 – Excess neurobehavioral 5 – 6% disorders attributable to 4 – secondhand smoke (SHS) exposure in the home. 3 – 2 – 1 – 0
    • Secondhand Smoke Exposure and Neurobehavioral Disorders Among Children in the United States Kabir, Pediatrics 2011;128:263 PREVALENCE OF (exposed vs nonexposed)20 –18 –16 –14 – 15.1%12 – 13.0%10 –08 – 8.7%06 – 7.2%04 – 5.5% 2.8%02 – 0 LEARNING ATTENTION- BEHAVIORAL AND DISABILITIES DEFICIT/HYPERACTIVITY CONDUCT DISORDER DISORDERS
    • Secondhand Smoke Exposure and Neurobehavioral Disorders Among Children in the United States Children exposed to SHS at home had a 50% increased odds of2011;128:263 Kabir, Pediatrics having ≥2 childhood neurobehavioral disorders PREVALENCE OF (exposed vs nonexposed)20 – compared with children who were18 – not exposed to SHS.16 –14 – 15.1%12 – 13.0%10 –08 – 8.7%06 – 7.2%04 – 5.5% 2.8%02 – 0 LEARNING ATTENTION- BEHAVIORAL AND DISABILITIES DEFICIT/HYPERACTIVITY CONDUCT DISORDER DISORDERS
    • Parental Smoking and Vascular Damage in Their 5-year-old Children Geerts, Pediatrics 2012;129;45 Video still from the carotid artery intima-media thickness Birth cohort. (CIMT) measurement. Smoking of parents during pregnancy. 259 participating children 5 years of age. Children‟s carotid artery intima-media thickness (CIMT) and arterial wall distensibility were measured by using ultrasonography.
    • Parental Smoking and Vascular Damage in Their 5-year-old Children Geerts, Pediatrics 2012;129;45 Video still from the carotid artery intima-media thickness Birth cohort. (CIMT) measurement. Smoking of parents during pregnancy. 259 participating children 5 years of age. Children‟s carotid artery Diameter and intima- intima-media thickness media thickness on the (CIMT) and arterial wall far wall is automatically distensibility were measured detected by using ultrasonography. and measured.
    • Parental Smoking and Vascular Damage in Their 5-year-old Children Geerts, Pediatrics 2012;129;45 Children of mothers who had Birth cohort. smoked throughout pregnancy had 18.8 µm thicker CIMT Smoking of parents during (P=0.04) and 15% lower pregnancy. distensibility (P =0.02) after 259 participating children adjustment for child‟s age, 5 years of age. maternal age, gender, and breastfeeding. Children‟s carotid artery intima-media thickness (CIMT) and arterial wall distensibility were measured by using ultrasonography.
    • Parental Smoking and Vascular Damage in Their 5-year-old Children Geerts, Pediatrics 2012;129;45 Children of mothers who had Birth cohort. smoked throughout pregnancy The associations had 18.8 µm thicker CIMT Smoking of parents during were not found (P=0.04) and 15% lower pregnancy. in children of distensibility (P =0.02) after mothers who had not 259 participating children adjustment for child‟s age, smoked of age. 5 years in pregnancy maternal age, gender, and breastfeeding. but had smoked Children‟s carotid artery thereafter. intima-media thickness (CIMT) and arterial wall distensibility were measured by using ultrasonography.
    • Parental Smoking and Vascular Damage in Their 5-year-old Children Geerts, Pediatrics 2012;129;45 If both parents had smoked Birth cohort. during pregnancy, with 27.7 mm thicker Smoking of parents during CIMT (95%) and pregnancy. 21% lower distensibility. 259 participating children 5 years of age. Children‟s carotid artery intima-media thickness (CIMT) and arterial wall distensibility were measured by using ultrasonography.
    • Parental Smoking and Vascular Damage in Their 5-year-old Children Geerts, Pediatrics 2012;129;45Difference in CIMT (A) and distensibility (B) in children bysmoking habits of mother in pregnancy and current smoking
    • Parental Smoking and Vascular Damage in Their 5-year-old Children Geerts, Pediatrics 2012;129;45Dose of tobacco smoke exposure in pregnancy and difference in CIMT (A) and distensibility (B) in the children
    • Parental Smoking and Vascular Damage in Their 5-year-old Children Geerts, Pediatrics 2012;129;45Paternal and maternal smoking during pregnancy and vascular outcome in their children.
    • Parental Smoking and the Risk of Middle Ear Disease in Children. Jones L, APAM 2012;166:18 OR for middle ear disease in children 2 – Systematic review 1.62 and meta-analysis. 1 – 1.37 Association between secondhand tobacco smoke and middle ear disease 0 in children. maternal any household member smoking living with a smoker
    • Parental Smoking and the Risk of Middle Ear Disease in Children. Jones L, APAM 2012;166:18 Risk for surgery 2 – 1.86 1.83 Systematic review and meta-analysis. 1 – Association between secondhand tobacco smoke and middle ear disease 0 in children. maternal paternal living with a smoker
    • Parental Smoking and the Risk of Middle Ear Disease in Children. Jones L, APAM 2012;166:18 Risk for surgery Exposure to 2 – SHTS, particularly to smoking by the 1.86 1.83 Systematic review mother, significantly and meta-analysis. of increases the risk 1 – Middle Ear Disease Association between in childhood; this risk secondhand tobacco is particularly strong smoke and requiring for MED middle ear disease surgery 0 in children. maternal paternal living with a smoker
    • Secondhand Smoke Exposure in Cars Among Middle and High School Students—United States, 2000–2009 King, Pediatrics 2012;129;446 % children exposed to secondhand smoke in car 100 –Students in grades 90 – p<0.001 6 to 12. 80 – 82.3% 70 – 75.3% 60 –Trends in 50 – secondhand smoke 40 – (SHS) exposure in 30 – a car. 20 – 10 – 0 2000 2009
    • Secondhand Smoke Exposure in Cars Among Middle and High School Students—United States, 2000–2009 King, Pediatrics 2012;129;446 % children exposed to SHS exposure in cars secondhand smoke in car 100 – decreased significantlyStudents in grades among US middle and 90 – p<0.001 6 to 12. high school students 80 – 82.3% from 2000 to 2009. 70 – 75.3% 60 –Nevertheless, in 2009, Trends in 50 – over 1/5 of secondhand smoke 40 – nonsmoking students (SHS) exposure in 30 – a car. exposed to were 20 – SHS in cars. 10 – 0 2000 2009
    • Exposure to parental and sibling smoking and the risk of smoking uptake in childhood and adolescence: a systematic review and meta-analysis Leonardi-Bee Thorax 2011;66:847 OR of uptake of smoking in children 3 – 2.19 2 –Meta-analyses 1.72 of 58 studies. 1.66 1 – At least one Smoking Smoking
    • Exposure to parental and sibling smoking and the risk of smoking uptake in childhood and adolescence: a systematic review and meta-analysis Leonardi-Bee Thorax 2011;66:847 OR of uptake of smoking in children 3 – 2.73 2.3 2 –Meta-analyses of 58 studies. 1 – Both parents Smoking by
    • Exposure to parental and sibling smoking and the risk of smoking uptake in childhood and adolescence: a systematic review and meta-analysis Leonardi-Bee Thorax 2011;66:847 OR of uptake of smoking in children It is estimated that, 3 – in England and Wales, 2.73 around 17000 young people take up smoking 2.3 by the age of 15 each 2 –Meta-analyses year as a consequence of 58of exposure studies. to household smoking. 1 – Both parents Smoking by
    • Smoking inpregnancy
    • Promoting Tobacco to Women of Reproductive Age Harms Fetuses. Farber H, Chest 2012;141:839 In utero tobacco smoke exposure has been repeatedly found to be associated with increased risk for premature birth, low birth weight, and sudden infant death syndrome. In utero tobacco smoke exposure only, in utero and postnatal smoke exposure, and postnatal smoke exposure all associated with increased risk of wheezing in the offspring compared with those of nonsmoking mothers.
    • Promoting Tobacco to Women of Reproductive Age Harms Fetuses. Farber H, Chest 2012;141:839 Smoking cessation either before pregnancy or early in gestation among women who are tobacco dependent can minimize the harm to their offspring. Tobacco-dependence treatment medications are preferable to continued in utero smoke exposure, which has well-defined harms to the fetus.
    • Promoting Tobacco to Women of Reproductive Age Harms Fetuses. Farber H, Chest 2012;141:839 Smoking cessation either before pregnancy or early in gestation among women who are tobacco dependent can minimize the harm to their offspring. and young women do not take up When girls smoking, their future offspring will be protected from these harms. Tobacco-dependence treatment medications are preferable to continued in utero smoke exposure,tobacco-dependenceharms When physicians offer which has well-defined to the fetus. treatment to women before they get pregnant or early in their pregnancy, harm can be reduced
    • Promoting Tobacco to Women of Reproductive Age Harms Fetuses. Farber H, Chest 2012;141:839 Smoking cessation either before pregnancy or early in gestation among women who are tobacco dependent can minimize the harm to their offspring. Tobacco-dependence treatment medications are preferable to continued in utero smoke exposure, which has well-defined harms to the fetus. Reduction of smoking in women of reproductive age needs to be a public health priority.
    • Fetal Exposure to Maternal and Paternal Smoking and the Risks of Wheezing in Preschool Children Duijts L, Chest 2012;141:876Background: Previous studies have suggested thatfetal smoke exposure is associated with increased risks ofwheezing during childhood.We examined the associations of parental smoking duringpregnancy with wheezing in preschool children and whetherthese associations are explained by postnatal smoke exposureor small for gestational age at birth.
    • Fetal Exposure to Maternal and Paternal Smoking and the Risks of Wheezing in Preschool Children Duijts L, Chest 2012;141:876 OR for frequent wheezing at age 3 – Parental smoking prospectively assessed by questionnaires. 2 – 2.19 1 – 1.64 1.64 Wheezing reported at 1 to 4 years. 00 4,574 subjects. age 1 age 2 age 3 In children exposed to continued maternal smoking in pregnancy
    • Fetal Exposure to Maternal and Paternal Smoking and the Risks of Wheezing in Preschool Children Duijts L, Chest 2012;141:876 Associations of continued maternal smoking during pregnancy and postnatal secondhand smoke exposure with wheezing at age 2 to 4 yrs *p< 0.05 ** p < 0.01
    • Fetal Exposure to Maternal and Paternal Smoking and the Risks of Wheezing in Preschool Children Duijts L, Chest 2012;141:876 Associations of continued maternal smoking during pregnancy and postnatal secondhand smoke exposure with wheezing at age 2 to 4 yrs *p< 0.05 ** p < 0.01 Compared with children who were not exposed to tobacco smoking during fetal life or early childhood, those who were exposed to smoke during fetal life only had higher risks of wheezing at ages 3 and 4 years (OR 1.65 and 1.78 respectively)
    • Fetal Exposure to Maternal and Paternal Smoking and the Risks of Wheezing in Preschool Children Duijts L, Chest 2012;141:876 Associations of continued maternal smoking during pregnancy and SGA at birth with wheezing until age 4 yrs *p< 0.05 ** p < 0.01
    • Fetal Exposure to Maternal and Paternal Smoking and the Risks of Wheezing in Preschool Children Duijts L, Chest 2012;141:876 Associations of continued maternal smoking during pregnancy and SGA at birth with wheezing until age 4 yrs *p< 0.05 ** p < 0.01 Children exposed to tobacco smoke only during pregnancy had higher risks of wheezing for all ages compared with children who were not exposed and not small for gestational age
    • Fetal Exposure to Maternal and Paternal Smoking and the Risks of Wheezing in Preschool Children Duijts L, Chest 2012;141:876 Associations of continued maternal smoking during pregnancy and SGA at birth with wheezing until age 4 yrs Fetal exposure to continued maternal *p< smoking is associated with increased0.05 ** p < risks of wheezing in preschool children. 0.01 Diminishing maternal smoking before conception or in early pregnancy is likely to have the greatest impact on reducing childhood wheezing
    • Persistent Asthma After In Utero Tobacco Exposure Akuete Pediatrics 2011;128:e623 OR for persistent In utero tobacco asthma 4.0 – smoke exposure. Childhood 3.0 – 3.57 2.0 – p=0.029 persistent asthma in 295 Mexican, 1.0 - Puerto Rican, and black children. 0.0 Exposure to in utero tobacco smoke
    • Persistent Asthma After In Utero Tobacco Exposure Akuete Pediatrics 2011;128:e623 OR in children exposed to 04 – in utero tobacco smoke In utero tobacco 3.85 03 – p=0.015 smoke exposure. 2.77 2.73 02 – p=0.048 p=0.046 Childhood persistent asthma in 295 Mexican, 01 – Puerto Rican, and black children. 00 Nocturnal Daily Emergency symptoms asthma department symptoms visits
    • Maternal smoking during pregnancy and offspring growth in childhood: 1993 and 2004 Pelotas cohort studies Matijasevich Arch Dis Child 2011;96:513 • Maternal smoking during Population-based pregnancy was associated with birth cohort reduced z scores of studies in Pelotas, length/height-for-age at each Brazil, in 1993 and follow-up. 2004. • Children older than 3 months born Followed up at to smoking women showed a 3, 12, 24 and 48 higher body mass index-for-age months. z score than children of nonsmoking women.
    • Maternal smoking during pregnancy and offspring growth in childhood: 1993 and 2004 Pelotas cohort studies Matijasevich Arch Dis Child 2011;96:513 • Maternal smoking during Population-based strongly The results pregnancy was associated with birth cohort support reduced z scores of the hypothesis that studies in Pelotas, length/height-for-age at each maternal smoking during Brazil, in 1993 and follow-up. 2004. pregnancy • Children older than 3 months born impairs linear growth Followed up at 3, overweight to smoking women showed a and promotes 12, 24 and 48 in higher body mass index-for-age months. childhood. z score than children of nonsmoking women.
    • Nicotine Replacement Therapy During Pregnancy And Infantile Colic in the Offspring Milidou, Pediatrics 2012;129;e652 Wessel‘s criteria for infantile colic 63 128 live-born singletons. Wessel defined infantile colic as paroxysms of crying and fussing Nicotine exposure for more than 3 hours per day during pregnancy. for more than 3 days per week for more than 3 weeks in an otherwise healthy Infantile colic and well-fed infant. symptoms at 6 months of age. Wessel MA, Cobb JC, Jackson EB, Harris GS, Jr, Detwiler AC. Paroxysmal fussing in infancy, sometimes called colic. Pediatrics. 1954;14(5):421–435
    • Nicotine Replacement Therapy During Pregnancy And Infantile Colic in the Offspring Milidou, Pediatrics 2012;129;e652 % infants fulfilled Wessel‘s modified criteria for infantile colic 63 128 live-born 1.0 – singletons. 0.9 – 0.8 – Nicotine exposure 0.7 – 7.9% during pregnancy. 0.6 – 0.5 – Infantile colic 0.4 – symptoms at 6 0.3 – months of age. 0.2 – 0.1 – 0.0 0
    • Nicotine Replacement Therapy During Pregnancy And Infantile Colic in the Offspring Milidou, Pediatrics 2012;129;e652 OR for infantile colic 3 – compared to unexposed 63 128 live-born singletons. 2 – Nicotine exposure during pregnancy. 1.6 1.6 1 – 1.3 Infantile colic symptoms at 6 months of age. 0 NRT users smokers women who both smoked(NRT=nicotine replacement therapy) and used NRT
    • Nicotine Replacement Therapy During Pregnancy And Infantile Colic in the Offspring Milidou, Pediatrics 2012;129;e652 OR for infantile colic Some authors argue –that the associationunexposed 3 componed to between 63 128 live-born infantile colic is entirely attributable smoking and singletons. to uncontrolled confounding by factors related to smoking behavior, such as social class. 2 – Nicotine exposure study the 2 models, adjusted In our during pregnancy. and unadjusted for socioeconomic status, yielded 1.6 1.6 1.3 similar results. The magnitude of association between 1 – Infantile colic nicotine exposure and infantile colic was symptoms at 6 similar across strata of months of age. socioeconomic status categories. 0 NRT users smokers women who both smoked(NRT=nicotine replacement therapy) and used NRT
    • Nicotine Replacement Therapy During Pregnancy And Infantile Colic in the Offspring Milidou, Pediatrics 2012;129;e652 OR for infantile colic 3 – componed to unexposed The dose-response like association seen between level 63 128 live-born singletons. exposure and risk for infantile colic might of nicotine indicate a causal link. In addition, NRTusers in our 2 – Nicotine exposure similar to the unexposed population sample were quite during pregnancy. other characteristics, which reduces with respect to 1.6 the risk of confounding. Even so, we cannot rule out 1.6 1 – 1.3 unmeasured or residual confounding due to our Infantile colic symptoms at 6 observational study design. months of age. 0 NRT users smokers women who both smoked(NRT=nicotine replacement therapy) and used NRT
    • Smokingandasthma
    • Prenatal and passive smoke exposure and incidence ofasthma and wheeze: systematic review and meta-analysis Burke Pediatrics 2012;129:735 % increased risk of incident wheezing 70 – 70% 60 – 50 –  79 prospective 40 – studies. 30 – 30% 20 – 10 – 0 Exposure to pre- or postnatal passive smoke
    • Prenatal and passive smoke exposure and incidence ofasthma and wheeze: systematic review and meta-analysis Burke Pediatrics 2012;129:735 % increased risk of incident asthma 90 – 85% 80 – 70 – 60 –  79 prospective 50 – studies. 40 – 30 – 20 – 21% 10 – 0 Exposure to postnatal passive smoke
    • Prenatal and passive smoke exposure and incidence ofasthma and wheeze: systematic review and meta-analysis Burke Pediatrics 2012;129:735 OR for wheeze in children aged ≤2 yrs 2 –  79 prospective studies. 1 – 1.70 0 Exposure to postnatal passive smoke
    • Prenatal and passive smoke exposure and incidence ofasthma and wheeze: systematic review and meta-analysis Burke Pediatrics 2012;129:735 OR for asthma in children aged ≤2 yrs 2 – 1.85  79 prospective studies. 1 – 0 Exposure to pre-natal passive smoke
    • Prenatal and passive smoke exposure and incidence ofasthma and wheeze: systematic review and meta-analysis Burke Pediatrics 2012;129:735 OR for asthma in children aged ≤2 yrs Preventing parental 2 – smoking 1.85  79 prospective is crucially important studies. to the prevention 1 – of asthma. 0 Exposure to pre-natal passive smoke
    • Comparison of Biomarkers and Parent Report of Tobacco Exposure to Predict Wheeze Spanier, J Ped 2011;159:776 % children exposed to tabacco smoke 70 –  398 mother-infant dyads enrolled 60 – during the second 50 – 61% trimester of pregnancy. 40 – 30 –  Followed through age 2 years. 20 – 26% 10 – 0 Parent report Cotinine level
    • Comparison of Biomarkers and Parent Report of Tobacco Exposure to Predict Wheeze Spanier, J Ped 2011;159:776 % children exposed to tabacco smoke 70 –  398 mother-infant a Serum cotinine, dyads enrolled of biomarker 60 – during the second tobacco exposure, 50 – 61% trimester of pregnancy. strongly was more 40 – associated with wheeze than  Followed through 30 – parent-reported age 2 years. 20 – 26% exposure. 10 – 0 Parent report Cotinine level
    • Comparison of Biomarkers and Parent Report of Tobacco Exposure to Predict Wheeze Spanier, J Ped 2011;159:776 OR for wheeze 3–  398 mother-infant dyads enrolled during the second 2– 2.6 trimester of pregnancy. .1 –  Followed through age 2 years. 0 Children of mothers in the 95th percentile compared with mothers in the fifth percentile of tobacco exposure
    • Defective epithelial barrier function in asthma Xiao JACI 2011;128:549BackgroundThe bronchial epithelium forms the interface with the externalenvironment and is pivotally involved in controlling tissuehomeostasis through provision of a physical barriercontrolled by tight junction (TJ) complexes.ObjectivesTo explain the link betweenenvironment exposures and airway vulnerability,we hypothesized that epithelial TJs are abnormal in asthma,leading to increased susceptibility to environmental agents.
    • Defective epithelial barrier function in asthma Xiao JACI 2011;128:549 Immunofluorescence staining of whole mount bronchial biopsies by using confocal microscopy (Zonula Occludens-1 stained green, Nuclei stained blue). Localization of Tight Junctions in bronchial biopsies and differentiated epithelial cultures. Electron microscopy of immunostaining. Baseline permeability and the effect of cigarette smoke.
    • Defective epithelial barrier function in asthma Xiao JACI 2011;128:549 Immunofluorescence staining of whole mount bronchial biopsies by using confocal microscopy (Zonula Occludens-1 stained green, Nuclei stained blue). Localization of Tight Junctions in bronchial biopsies and biopsies Bronchial from asthmatic differentiated epithelial cultures. subjects displayed patchy disruption Electron microscopy of immunostaining. of TJs. Baseline permeability and the effect of cigarette smoke.
    • Defective epithelial barrier function in asthma Xiao JACI 2011;128:549 Analysis of TJs in differentiated BEC cultures. Localization of Tight Junctions in bronchial biopsies and differentiated epithelial cultures. Electron microscopy of immunostaining. Baseline permeability and the effect of TJs; tight junctions cigarette smoke. BEC; bronchial epithelial cells ZO; zonula occuldens
    • Defective epithelial barrier function in asthma Xiao JACI 2011;128:549 Transepithelial electrical resistance. Localization of Tight Junctions in bronchial biopsies and differentiated epithelial cultures. Electron microscopy of immunostaining. Baseline permeability and the effect of cigarette smoke.
    • Defective epithelial barrier function in asthma Xiao JACI 2011;128:549 Transepithelial electrical resistance. Transepithelial electrical resistance was Localization of Tight significantly lower (p< 0.05) Junctions in bronchial in cultures biopsies and asthmatic donors from (n=43) than from normal differentiated epithelial cultures. (n=40). controls Electron microscopy asthmatic Cultures from of immunostaining. also more donors were sensitive to disruption Baseline by cigarette smoke permeability and the effect of extract. cigarette smoke.
    • Interaction between filaggrin null mutations and tobacco smoking in relation to asthma Berg JACI 2012;129:374 4.0 – OR for asthma in FLG null mutations 3471 adults from vs wild type. general population. 3.5 - 3.70 3.0 – Lung function 2.5 – and IgE levels to inhalant allergens. 2.0 – 1.5 – 1.96 Filaggrin 1.02 1.57 1.0 – (FLG) null mutations. 0.5 - 0.0 R501X and Never Former ≤15 g/d ≥15 g/d 2282del4. current SMOKING
    • Interaction between filaggrin null mutations and tobacco smoking in relation to asthma Berg JACI 2012;129:374 4.0 – OR for asthma in FLG null mutations A significant 3471 adults from vs wild type. interaction general population. 3.5 - 3.70 3.0 – was found Lung function 2.5 – between and IgE levels to inhalant allergens. 2.0 – FLG null 1.96 mutations Filaggrin 1.5 – 1.02 1.57 1.0 – (FLG) nulland mutations. status 0.5 - smoking (p=0.02). R501X and 0.0 Never Former ≤15 g/d ≥15 g/d 2282del4. current SMOKING
    • Smoking, environmental tobacco smoke, and aspirin exacerbated respiratory disease Chang, Ann Allergy Asthma Immunol 2012;108:14 in case patients ever smoking actively OR for AERD To investigate whether 2 – active smoke or environmental tobacco smoke (ETS) exposures are associated with an 1.54 increased risk of aspirin- 1 – exacerbated respiratory disease (AERD). 260 patients with AERD. 0 vs controls
    • Smoking, environmental tobacco smoke, and aspirin exacerbated respiratory disease Chang, Ann Allergy Asthma Immunol 2012;108:14 OR for AERD 4 – To investigate whether active smoke or environmental tobacco 3 – 3.46 smoke (ETS) exposures are associated with an 2 – increased risk of aspirin- exacerbated respiratory 1 – disease (AERD). 00 260 patients with AERD. Childhood ETS exposure
    • Smoking, environmental tobacco smoke, and aspirin exacerbated respiratory disease Chang, Ann Allergy Asthma Immunol 2012;108:14 OR for AERD 6 – To investigate whether active smoke or 5 – environmental tobacco 4 – 5.09 smoke (ETS) exposures are associated with an 3 – increased risk of aspirin- exacerbated respiratory 2 – + 1 – disease (AERD). 00 260 patients with AERD. Exposed to ETS during both childhood and adulthood
    • Smoking, environmental tobacco smoke, and aspirin exacerbated respiratory disease Chang, Ann Allergy Asthma Immunol 2012;108:14 Potential explanation1) Childhood ETS exposure is likely to have cumulative effects on respiratory membranes with persistent damage and inflammation.2) Many AERD patients have documented pansinusitis.3) Early life influences adultonset disease in asthma which may extend to AERD (Barker‟s Hypothesis).4) Environmental signals during childhood may prime the patient via an epigenetic pathway; thus, childhood ETS may have a greater effect than adult exposure.
    • A Randomized Trial of Air Cleaners and a Health Coach to Improve Indoor Air Quality for Inner-City Children With Asthma and Secondhand Smoke Exposure Butz APAM 2011;165:741 Mean differences in fine (aerodynamic diameter of 2.5 μm) and coarse (aerodynamic diameter of 2.5 – 10 μm) particulate matter (PM2.5 and PM2.5-10) concentrations from the 6-month follow-up, minus the baseline concentrations in the control compared with both air cleaner groups Children with asthma, residing with a smoker. Air cleaners(n=41) Air cleaners + health coach (n=41) Delayed air cleaner (control, n=44).
    • A Randomized Trial of Air Cleaners and a Health Coach to Improve Indoor Air Quality for Inner-City Children With Asthma and Secondhand Smoke Exposure Butz APAM 2011;165:741 Mean differences in fine (aerodynamic diameter of 2.5 μm) and coarse (aerodynamic diameter of 2.5 – 10 μm) particulate matter (PM2.5 and PM2.5-10) concentrations from the 6-month follow-up, minus the baseline concentrations in the control compared with both air cleaner groups Children with asthma, residing with a No differences smoker. were noted in Air cleaners(n=41) or air nicotine Air cleanerscotinine urine + health coach (n=41) concentrations. Delayed air cleaner (control, n=44).
    • A Randomized Trial of Air Cleaners and a Health Coach to Improve Indoor Air Quality for Inner-City Children With Asthma and Secondhand Smoke Exposure Butz APAM 2011;165:741 Symptom-free days during the past 2 weeks. 1.5 – Children with asthma, residing with a 1.36 smoker. 1.0 – Air cleaners(n=41) p=0.03 Air cleaners + 0.5 – health coach (n=41) Delayed air cleaner (control, n=44). 00 0.24 Air cleaner Control groups group
    • A Randomized Trial of Air Cleaners and a Health Coach to Improve Indoor Air Quality for Inner-City Children With Asthma and Secondhand Smoke Exposure Butz APAM 2011;165:741 Symptom-free days during the past 2 weeks. The use of air cleaners 1.5 – can result in: Children with asthma, residing with a reduction • a significant 1.36 smoker. indoor PM in 1.0 – concentrations; • cleaners(n=41) Air a significant increase p=0.03 in symptom-free days. Air cleaners + it is However 0.5 – not coach (n=41) healthenough to prevent exposure to secondhand Delayed air cleaner smoke. (control, n=44). 00 0.24 Air cleaner Control groups group
    • Impact of cigarette smoke exposure on host–bacterialpathogen interactions. Garmendia J, Eur Respir J 2012;39:467 Molecular mechanisms involved in chronic obstructive pulmonary disease (COPD) progression. Three major host alterations characteristic of COPD progression, fibrosis, emphysema and mucus hypersecretion, are shown.
    • Impact of cigarette smoke exposure on host–bacterialpathogen interactions. Garmendia J, Eur Respir J 2012;39:467A fourth characteristic of COPD progression, lower airway colonisation by opportunisticpathogens, is stated (bottom). Microbial persistency is relevant because it greatlycontributes to deleterious amplification of COPD features. The main host cells involved inCOPD patient airways, epithelial cells, alveolar macrophages (AMs), neutrophils and CD8+lymphocytes, are shown. Cigarette smoke activates epithelial cells to produce inflammatorymediators, activating and/or recruiting AMs and neutrophils. Epithelial cells also secretethe local fibrosis inducer transforming growth factor (TGF)-β. Chemokines produced byepithelial cells and AMs activate CD8+ lymphocytes, which release the emphysemamediators perforin and granzyme. AMs secrete neutrophil chemoattractants and releaseproteases. Matrix metalloproteinase (MMP)-9 activates the fibrosis inducer TGF- β andcauses elastolysis, either directly or by α1-antitrypsin (AT) inactivation. Proteasesproduced by AMs and neutrophils promote emphysema. Together withproteases, neutrophils secrete inflammatory mediators and granule contents. Neutrophilchemoattractants are produced directly by AMs and epithelial cells, and by enzymaticactivity of the AM protease MMP-9. COPD patient airways display oxidative stress.Cigarette smoke itself contains high levels of reactive oxygen species (ROS), and bothAMs and neutrophils increase their respiratory burst in response to cigarette smoke. Highconcentrations of ROS and reactive nitrogen species have multiple consequences: 1)decreased antiprotease defences and proteolysis; 2) activation of nuclear factor (NF)-kBand neutrophil recruitment; 3) steroid resistance; 4) increased isoprostanes production;and 5) mucus hypersecretion. SLPI: secretory leukoprotease inhibitor.
    • Impact of cigarette smoke exposure on host–bacterialpathogen interactions. Garmendia J, Eur Respir J 2012;39:467 The vicious circle hypothesis of chronic obstructive pulmonary disease (COPD) progression
    • Impact of cigarette smoke exposure on host–bacterialpathogen interactions. Garmendia J, Eur Respir J 2012;39:467 Cigarette smoke is an external insult that damages respiratory tract immunity, allowing lower respiratory tract colonisation by microorganisms. Such colonisation is a starting point for a cyclic sequence of events that progressively contribute to a high level of chronic inflammation, tissue damage and fibrosis, together with persistent bacterial infection of the lower airways. Together, these processes continuously contribute to the nonreversible progression of the chronic respiratory disease.
    • Impact of cigarette smoke exposure on host–bacterialpathogen interactions. Garmendia J, Eur Respir J 2012;39:467 Cigarette smoke and host insensitivity to corticoids
    • Impact of cigarette smoke exposure on host–bacterialpathogen interactions. Garmendia J, Eur Respir J 2012;39:467Histone deacetylase (HDAC) reduction caused by cigarette smoke may accountfor an amplification of the inflammatory response (right) and insensitivity to theanti-inflammatory effect of corticoids (left).Cigarette smoke activates nuclear factor (NF)-kB in alveolar macrophages (right).Gene expression is activated by histone acetyltransferase (HAT)-mediated corehistone acetylation; histone acetylation of inflammatory gene promotersactivated by NF-kB is increased in chronic obstructive pulmonary disease.The increase in acetylation is due to a reduction of HDACs. HDACs reversehistone acetylation and switch off gene transcription. HDACs are inactivated byoxidative and nitrosative stress. Oxidative and nitrosative stress lead to theformation of peroxynitrite, which nitrosylates HDAC, leading to its degradation,resulting in low HDAC levels and, subsequently, in an amplification of theinflammatory response. HDAC reduction by cigarette smoke-induced oxidativestress impairs the response to corticoids. Glucocorticoids (GCs) bind GC receptor(GR) and recruit HDAC to activated inflammatory genes; by reversing theacetylation of those genes, their transcription is switched off and theinflammation is reduced (left). IL: interleukin; TNF: tumour necrosis factor;ROS: reactive oxygen species; NO: nitric oxide.
    • Smoking andPediatricians and Society
    • Physician Communication Regarding Smoking and Adolescent Tobacco Use Hum Pediatrics 2011;127:e1368 Knowledge of tobacco-related damage according to smoking status and physician communication. Higher scores indicate more knowledge. 5154 students. Adolescents‟ self-rated attitudes toward smoking, knowledge about smoking, intentions to smoke, tobacco use, and quitting behaviors.
    • Physician Communication Regarding Smoking and Adolescent Tobacco Use Hum Pediatrics 2011;127:e1368 Knowledge of tobacco-related damage according to smoking status and physician communication. Among current 5154 students. Higher scores indicate more knowledge. smokers, recalled physician Adolescents‟ self-ratedwas also advice attitudes toward associated with smoking, knowledge reduced intentions about to smoke in smoking, intentions 5 years. to smoke, tobacco use, and quitting behaviors.
    • Physician Communication Regarding Smoking and Adolescent Tobacco Use Hum Pediatrics 2011;127:e1368 Knowledge of tobacco-related damage according Advised teens were to smoking status and physician communication. Higher scores indicate more knowledge. 5154 students.plan to more likely to quit smoking in 6 months. Adolescents‟ Furthermore, teens who self-rated attitudes were screened by their toward smoking, physician reported knowledge about quit significantly more smoking, intentions attempts than those to who were neither smoke, tobacco use, and quitting screened nor advised. behaviors.
    • Cross-sectional association between smoking depictions in films and adolescent tobacco use nested in a British cohort study Waylen Thorax 2011;66:856 RR to initiate smoking 2 – 1.73 Exposure to smoking in films 1 – and smoking behaviour. 5166 15-years-old adolescents in the UK. 0 Adolescents in the highest exposure quartile than those in the lowest quartile
    • Cross-sectional association between smoking depictions in films and adolescent tobacco use nested in a British cohort study Waylen Thorax 2011;66:856 RR to initiate smoking 2 – Viewing smoking in films 1.73 Exposure increases to smoking in films 1 – the risk and smoking of smoking behaviour. onset. 5166 15-years-old 0 adolescents in the UK. Adolescents in the highest exposure quartile than those in the lowest quartile
    • Smoking in movies and adolescent smoking: cross-cultural study in six European countries Morgenstern Thorax 2011;66:875 % adolescents who had tried smoking 30 – 16551 pupils recruited in Germany, Iceland, Italy, the Netherlands, Poland 29% and Scotland. 20 – Mean age of 13.4 years. School-based surveys. 10 – Exposure to movie smoking estimated from the 250 top- grossing movies of each country. 0
    • Smoking in movies and adolescent smoking:cross-cultural study in six European countries Morgenstern Thorax 2011;66:875 % adolescents who had tried smoking 40 – 30 – 36% 29% 20 – 21% 10 – 14% OR = 1.3 OR = 1.6 OR = 1.7 0 Q1 Q2 Q3 Q4 Quartile (Q) of movie smoking exposure
    • Smoking in movies and adolescent smoking:cross-cultural study in six European countries Morgenstern Thorax 2011;66:875 % adolescents who smoking in smoking The link between had tried movies and adolescent smoking is robust and transcends different 40 – cultural contexts. 30 – 36% 29% 20 – 21% 10 – 14% OR = 1.3 OR = 1.6 OR = 1.7 0 Q1 Q2 Q3 Q4 Quartile (Q) of movie smoking exposure
    • Smoking in movies and adolescent smoking:cross-cultural study in six European countries Morgenstern Thorax 2011;66:875 %Limiting young people‘stried smoking adolescents who had exposure to movie smoking could have important 40 – public health implications. 30 – 36% 29% 20 – 21% 10 – 14% OR = 1.3 OR = 1.6 OR = 1.7 0 Q1 Q2 Q3 Q4 Quartile (Q) of movie smoking exposure
    • Aerobic exercise attenuates pulmonary injury induced by exposure to cigarette smoke Toledo A.C, Eur Respir J 2012;39:254 • Exercise attenuated the decrease in pulmonary elastance (p<0.01).experimental mouse model of chronic cigarette • Exercise substantially inhibited the smoke exposure increase in ROS in BAL fluid and 8-isoprostane expression in lung tissue induced by cigarette smoke. • Exercise significantly inhibited the divided into four groups decreases in IL-10 and (control, exercise, smoke CuZn superoxide dismutase induced by and smoke+exercise), exposure to cigarette smoke. for 24 weeks • Exercise also increased the number of cells expressing glutathione peroxidase.
    • Effects of physical activity on teen smoking cessation Horn Pediatrics 2011;128:e801 Teens (n= 233; 14 –19 yrs) Girls quit more successfully from West Virginia high with N-O-T compared with schools who smoked >1 cigarette in the previous BI (relative risk [RR]:> ∞) 30 days. 3 months after baseline, Randomly and assigned to brief intervention (BI), and boys responded better to Not on Tobacco (N-O-T) N-O-T+FIT than to BI (a proven teen cessation (RR=2–3) program), or N-O-T plus a physical activity module or to N-O-T (RR=1–2). (N-O-T+FIT). Quit rates 3 and 6 months after.
    • Effects of physical activity on teen smoking cessation Horn Pediatrics 2011;128:e801 Teens (n= 233; 14the yrs) Youths in –19 Girls quit more successfully from West Virginia high N-O-T+FIT group, with N-O-T compared with schools who smoked >1 compared with those cigarette in the previous BI (relative risk [RR]:> ∞) 30 days. in the N-O-T group, 3 months after baseline, Randomly and assigned had greater likelihood to brief intervention and boys responded better to (BI), of cessation (N- Not on Tobacco N-O-T+FIT than to BI (RR=1.48) O-T) (a proven teen (RR=2–3) cessation program), or N- at 6 months. O-T plus a physical or to N-O-T (RR=1–2). activity module (N-O- T+FIT). Quit rates 3 and 6 months after.
    • Effectiveness of a School Nurse–Delivered Smoking- Cessation Intervention for Adolescents Pbert Pediatrics 2011;128:926 35 high schools OR to be abstinent per 4 visits with the school self-report at 3 months nurse Adolescents (n=1068) 2 - 1.90 who reported past 30-day smoking and interest in quitting 1 – baseline and at 3 and 12 months p= 0.017 0 saliva samples for Participants biochemical validation
    • Effectiveness of a School Nurse–Delivered Smoking- Cessation Intervention for Adolescents Pbert Pediatrics 2011;128:926 35 high schools OR to be abstinent per 4 visits with the school self-report at 3 months nurse At 12(n=1068) Adolescents months 2 - who reported were no there interest in 1.90 past 30-day smoking and differences. quitting 1 – baseline and at 3 and 12 months p= 0.017 0 saliva samples for Participants biochemical validation
    • Effectiveness of a School Nurse–Delivered Smoking- Cessation Intervention for Adolescents Pbert Pediatrics 2011;128:926 35 high schools The difference OR to be abstinent per at 3 months was driven 4 visits with the school self-report at 3 months nursequit rates in male by students Adolescents (n=1068) 2 - (15.0% [intervention] 1.90 who reported past 30-day vs 4.9% [control]; smoking and interest in OR: 3.23, (p=.001); quitting 1 – baselinethere was and at 3 and no intervention effect 12 months p= 0.017 in female students. 0 saliva samples for Participants biochemical validation
    • The Efficacy of Motivational Interviewing Versus Brief Advice for Adolescent Smoking Behavior Change Audrain-McGovern Pediatrics 2011;128:e101 OR for adolescents who Efficacy of motivational received MI to try to interviewing (MI) compared quit smoking with structured brief advice 1.0 – (SBA) for adolescent smoking 0.9 – (n=355) behavior change. 0.8 – 0.7 – Attempts to reduce and to quit 0.6 – 0.5 – smoking, smoking reduction, 0.4 – and cotinine-validated 7-day point-prevalence smoking 0.3 – 0.2 – 0.41 abstinence at the end of 0.1 – p=0.03 treatment (week 12) and the 0 vs adolescents 24-week follow-up. who received SBA
    • The Efficacy of Motivational Interviewing Versus Brief Advice for Adolescent Smoking Behavior Change Audrain-McGovern Pediatrics 2011;128:e101 OR for adolescents who Efficacy of motivational received MI to try to interviewing (MI) compared adolescents quit smoking with structured brief advice who received MI showed 1.0 – (SBA) for adolescent smoking (n=355) behavior change. in a greater reduction 0.9 – 0.8 – cigarettes smoked per 0.7 – day than adolescents Attempts to reduce and to quit 0.6 – 0.5 – smoking, smoking reduction, who received SBA 0.4 – and cotinine-validated 7-day (5.3 vs 3.3 fewer point-prevalence smoking cigarettes per day). 0.3 – 0.2 – 0.41 abstinence at the end of 0.1 – p=0.03 treatment (week 12) and the 0 vs adolescents 24-week follow-up. who received SBA
    • The Efficacy of Motivational Interviewing Versus Brief Advice for Adolescent Smoking Behavior Change Audrain-McGovern Pediatrics 2011;128:e101 Comparison of MI and SBA Treatment Approaches
    • The Efficacy of Motivational Interviewing Versus Brief Advice for Adolescent Smoking Behavior Change Audrain-McGovern Pediatrics 2011;128:e101Conclusion:The effects of MI on adolescentsmoking behavior change aremodest, and MI may best fitwithin a multicomponent smokingcessation treatment approach inwhich behavior change skills cansupport and promote smokingbehavior change decisions.
    • Increasing the age for the legal purchase of tobacco in England: impacts on socio-economic disparities in youth smoking Millett Thorax 2011;66:862BackgroundThe minimum age for the legal purchase of tobacco increasedfrom 16 to 18 years in England, Scotland and Wales on1 October 2007.The authors examined the impact of this legislation ondisparities in smoking behaviour and access to cigarettesamong youth in England.
    • Increasing the age for the legal purchase of tobacco in England: impacts on socio-economic disparities in youth smoking Millett Thorax 2011;66:862 OR for regular smoking 1.0 – Smoking, Drinking and Drug Use Survey, a national survey 0.5 – 0.67 of 11-15 years olds. p=0.0005 0.0 Increasing the minimum age for purchase from 16 to 18 yrs
    • Increasing the age for the legal purchase of tobacco in England: impacts on socio-economic disparities in youth smoking Millett Thorax 2011;66:862 OR for regular smoking Increasing the age 1.0 – for the legal purchase of tobacco was associated with Smoking, Drinking smoking reduced regular and Drug Use Survey, among youth in England a national survey 0.5 – 0.67 and appeared to have of 11-15 years olds. a similar impact p=0.0005 in different socio-economic groups. 0.0 Increasing the minimum age for purchase from 16 to 18 yrs
    • Biomarkers of early respiratory effects in smoking adolescents Van Miert ERJ 2011;38:1287Noninvasive biomarkers can be used to evaluate airways damagecaused by tobacco smoke, but studies so far have only involved adult smokers.In this study, we evaluated whether such biomarkers can detect early respiratory effects in adolescents passively or actively exposed to tobacco smoke.
    • Biomarkers of early respiratory effects in smoking adolescents Van Miert ERJ 2011;38:1287 845 adolescents. Exhaled nitric oxide and various The levels of epithelial markers in nasal lavage fluid (NALF) and serum, including exhaled NO and Clara cell protein (CC16) and of CC16 in NALF surfactant protein (SP)-D. were significantly Smoking habits by questionnaire. decreased Four groups of equal size in the group (n=36), of nonsmokers, passive of heavy smokers. smokers, light smokers (<5 cigarettes/day) and heavy smokers (≥5
    • Biomarkers of early respiratory effects in smoking adolescents Van Miert ERJ 2011;38:1287 845 adolescents. There were no Exhaled nitric oxide and various significant changes epithelial markers in nasal lavage in serum CC16 and fluid (NALF) and serum, including Clara cell protein (CC16) and SP-D, which surfactant protein (SP)-D. suggests that the Smoking habits by questionnaire. deep lung epithelium had not Four groups of equal size (n=36), of nonsmokers, passive smokers, yet been affected light smokers (<5 cigarettes/day) by smoking. and heavy smokers (≥5 cigarettes/day).
    • Biomarkers of early respiratory effects in smoking adolescents Van Miert ERJ 2011;38:1287 Relationship between daily cigarette Adjusted Clara cell Adjusted nitric oxide consumption andprotein (CC16) level. (NO) levels in oral Nitric oxide (NO) in exhalate. exhaled air. p<0.05
    • Biomarkers of early respiratory effects in smoking adolescents Van Miert ERJ 2011;38:1287 Tobacco smoke can cause early changes between Relationship in the airways of adolescents with a cigarette Adjusted Clara cell Adjusted nitric oxide daily consumption andprotein (CC16) level. smoking history oral <1 pack-yr. (NO) in cumulative (NO) levels in of Nitric oxide exhalate. exhaled air. p<0.05
    • Parental Smoking Cessation to Protect Young Children: A Systematic Review and Meta-analysis Rosen, Pediatrics 2012;129 % parents quitting smoking Systematic review 30 – and meta-analysis. p=0.005 Effects of interventions that encourage parents of 20 – 23% infants or young children 18.4% to quit smoking for their 10 – children‟s benefit. 18 trials were included. 0 YES NO intervention
    • Parental Smoking Cessation to Protect Young Children: A Systematic Review and Meta-analysis Rosen, Pediatrics 2012;129 % parents quitting smoking Systematic review 30 – and meta-analysis. p=0.005 An additional 4% Effects of interventions that the intervention of encourage parents of 20 – 23% infants or young children parents quit 18.4% to quit smoking for their smoking. children‟s benefit. 10 – 18 trials were included. 0 YES NO intervention
    • Parental Smoking Cessation to Protect Young Children: A Systematic Review and Meta-analysis Rosen, Pediatrics 2012;129 OR for intervention program on parental quit rate stratified Systematic review according to the child age and meta-analysis. 2 – Effects of interventions that encourage parents of 1.57 infants or young children to quit smoking for their 1 – 1.14 children‟s benefit. 1 18 trials were included. p=0.006 00 0-1 yr 2-4 yr 4-17 yr
    • Parental Smoking Cessation to Protect Young Children: A Systematic Review and Meta-analysis Rosen, Pediatrics 2012;129 OR for intervention program on parental quit rate stratified Systematic review according to the child age and meta-analysis. 2 – Subgroups withsignificantinterventions Effects of intervention that encourage parents of 1.57 benefits were infants or young children to quit smokingaged children for their 1 – 1.14 4 to 17 years. children‟s benefit. 1 18 trials were included. p=0.006 00 0-1 yr 2-4 yr 4-17 yr
    • An Evaluation of a Clinical Approach to Staging Tobacco Addiction DiFranza, J Ped 2011;159:999 % subjects reporting 349 tobacco users in grades 9. withdrawal symptoms (wanting, craving, needing) Withdrawal symptoms. 100 - Dependence was measured by several validated measures, including the Hooked on 080 – 99.4% Nicotine Checklist, the 060 – Autonomy Over Tobacco Scale, and the modified 040 – Fagerström Tolerance 020 – Questionnaire. 000
    • An Evaluation of a Clinical Approach to Staging Tobacco Addiction DiFranza, J Ped 2011;159:999FagerströmToleranceQuestionnaire
    • An Evaluation of a Clinical Approach to Staging Tobacco Addiction DiFranza, J Ped 2011;159:999 % subjects reporting 349 tobacco users in grades 9. withdrawal symptoms (wanting, craving, needing) Withdrawal symptoms. Across the 100 - stages, from wanting to Dependence was measured by needing, several validated measures, including thestages were higher Hooked on 080 – 99.4% Nicotine Checklist,with associated the 060 – Autonomy Over Tobacco in significant increases the strength of Scale, and the modified 040 – addiction. Fagerström Tolerance 020 – Questionnaire. 000
    • An Evaluation of a Clinical Approach to Staging Tobacco Addiction DiFranza, J Ped 2011;159:999 % subjects reporting 349 tobacco users in grades 9. withdrawal symptoms (wanting, craving, needing) Withdrawal symptoms. Withdrawal symptoms Dependence in an orderly by develop was measured 100 - several validated wanting, sequence of measures, including the Hooked onwhich craving, and needing 080 – 99.4% represents a substantial Nicotine Checklist, the 060 – increase in tobacco Autonomy Over Tobacco Scale, andaddiction. the modified 040 – Fagerström Tolerance 020 – Questionnaire. 000
    • What makes for an effective stop-smoking service? Brose Thorax 2011;66:924 126890 treatment episodes in 24 stop-smoking services OR for success rate (SSSs) 2 – Intervention characteristics 1.75 and success rates 1.42 1.43 Varenicline, single nicotine replacement therapy (NRT) 1 – combination of 2 or more forms of NRT. Abstinence from smoking 4 weeks after the target quit date, verified by carbon 0 monoxide concentration in Single NRT Combination Group support vs no NRT and vs one-to-one expired air. medication varenicline vs support single NRT
    • What makes for an effective stop-smoking service? Brose Thorax 2011;66:924 126890 treatment episodes Smokers receiving in 24 stop-smoking services OR for success rate (SSSs) 2 – stop-smoking support from specialist clinics, Intervention characteristics 1.75 and success rates groups treatment in and varenicline or 1.42 1.43 Varenicline, single nicotine combination NRT are replacement therapy (NRT) 1 – more likely to or more combination of 2 succeed forms of NRT. receiving than those treatment in primary Abstinence from smoking 4 weeks after the targetand care, one-to-one quit date, verified by carbon 0 single NRT. Single NRT Combination Group support monoxide concentration in vs no NRT and vs one-to-one expired air. medication varenicline vs support single NRT
    • An Unexpected Consequence of Electronic Cigarette Use McCauley L, Chest 2012;141:1110 Exogenous lipoid pneumonia is a chronic inflammatory reaction to the deposition of lipid substances in the lung, typically as a result of aspiration or inhalation of oil-based products. Chest CT imaging typically shows bilateral alveolar consolidation and ground glass opacities, including the “crazy paving” pattern, in the dependent areas of the lungs. The presence of lipid-laden macrophages in sputum or BAL fluid helps to confirm the diagnosis. The symptoms and pathologic changes often completely resolve with the cessation of exposure; however, severe cases can progress to fibrosis and chronic respiratory failure.
    • An Unexpected Consequence of Electronic Cigarette Use McCauley L, Chest 2012;141:1110  A 42-year-old woman was admitted to the hospital with a 7-month history of dyspnea, productive cough, and subjective fevers.  The patient had recently started using electronic cigarettes (e-cigarettes), about 7 months prior.  CT images revealed extensive bilateral upper-and lower-lobe patchy ground glass pulmonary opacities in a “crazy paving” pattern.  BAL cytologic examination revealed abundant lipid-laden macrophages.
    • An Unexpected Consequence of Electronic Cigarette Use McCauley L, Chest 2012;141:1110 Representative CT images show the ―crazy paving‖ pattern of patchy ground glass superimposed on interlobular septal thickening. A, Bilateral upper lobes. B, Bilateral lower lobes.A B
    • An Unexpected Consequence of Electronic Cigarette Use McCauley L, Chest 2012;141:1110 Many public health authorities, the ―crazythe US pattern Representative CT images show including paving‖ Food and of patchy Administration, caution thatinterlobular and benefits Drug ground glass superimposed on the risks septal thickening. of A, Bilateral upper lobes. been adequately studied. e-cigarettes have not B, Bilateral lower lobes.A This case demonstrates an important heretofore B unrecognized health risk of e-cigarette use: exogenous lipoid pneumonia due to glycerin-based e-cigarettes.
    • • pollution
    • Does air pollution increase the effect of aeroallergens on hospitalization for asthma? Cakmak JACI 2012;129:228Effects of ambient aeroallergens on hospitalization for asthma between high and low air pollution days in 11 large Canadian cities. CO, Carbon monoxide; IQR, interquartile range; NO2, nitrogen dioxide; RR, relative risk; SO2, sulfur dioxide.
    • Does air pollution increase the effect of aeroallergens on hospitalization for asthma? Cakmak JACI 2012;129:228 Effects of ambient aeroallergensHospitalizations on for asthma hospitalization was asthma for enhanced between of on days high and low higher air pollution air pollution. days in 11 large Canadian cities. CO, Carbon monoxide; IQR, interquartile range; NO2, nitrogen dioxide; RR, relative risk; SO2, sulfur dioxide.
    • Does air pollution increase the effect of aeroallergens on hospitalization for asthma? Cakmak JACI 2012;129:228 Effects of ambient The aeroallergens adverse effect on several of hospitalization aeroallergens for asthma was greater on between days and higher high of low versus lower air pollution dayspollution. air in 11 large Canadian cities. CO, Carbon monoxide; IQR, interquartile range; NO2, nitrogen dioxide; RR, relative risk; SO2, sulfur dioxide.
    • Does air pollution increase the effect of aeroallergens on hospitalization for asthma? Cakmak JACI 2012;129:228 Effects of Minimizing ambient aeroallergens exposure on to hospitalization air asthma for pollution reduce between high and low allergic air pollution exacerbations days of11 large . in asthma Canadian cities. CO, Carbon monoxide; IQR, interquartile range; NO2, nitrogen dioxide; RR, relative risk; SO2, sulfur dioxide.
    • Does air pollution increase the effect of aeroallergens on hospitalization for asthma? Cakmak JACI 2012;129:228Theories to explain an aeroallergen–air pollution interaction•It has been hypothesized that damage to the airwaysby air pollutants might increase mucosal permeabilityand thereby penetration of allergens.•Metal components of fine particulate air pollutionmight enhance the allergic response.•Diesel exhaust particles have been shown toenhance the production of IgE specific.•This can be inhibited by antioxidants, suggesting thatthe adjuvant effect of the particles is mediated byreactive oxygen species.Whitekus M. J Immunol 2002;168:2560-7
    • Does air pollution increase the effect of aeroallergens on hospitalization for asthma? Cakmak JACI 2012;129:228Theories to explain an aeroallergen–air pollution interaction•Dieselexhaust particles might also facilitatetransportation of pollen antigens to the small airways.•Disruption of pollen grains by diesel exhaust particleswas observed by using scanning electron microscopy.•Through inhibiting ciliary beat frequency,diesel exhaust particles might reduceallergen clearance and prolong theallergic response.
    • Traffic-related air pollution and development ofallergic sensitization in children during the first 8 years of life Gruzieva JACI 2012;129:240 2500 children in the OR for pollen sensitization birth cohort at 4 years of age from Stockholm. 2.0 – Followed until 8 yrs of age. 1.5 – 1.83 1.0 – Outdoor concentrations 0.5 - of nitrogen oxides, a marker 0.0 ofexhaust For a 5th to 95th difference in particles, exposure to nitrogen oxides. and
    • The respiratory health effects of nitrogen dioxide inchildren with asthma Gillespie-Bennett ERJ 2011;38:303 Geometric mean 15 – NO2 levels µg/m3 Indoor nitrogen dioxide (NO2) emitted from 11.4 10 – unflued gas heating. Respiratory health of children. 05 – 7.4 0 INDOOR OUTDOOR
    • The respiratory health effects of nitrogen dioxide inchildren with asthma Gillespie-Bennett ERJ 2011;38:303 Higher indoor NO2 Geometric mean 15 – NO2 levels µg/m3 levels were associated Indoor nitrogen dioxide with greater daily (NO2) emitted from reports of lower 10 11.4 – unflued gas heating. and upper respiratorytract symptoms,of Respiratory health more children. frequent cough and 05 – 7.4 wheeze, and with a decrease FEV1. 0 INDOOR OUTDOOR
    • The respiratory health effects of nitrogen dioxide inchildren with asthma Gillespie-Bennett ERJ 2011;38:303 Geometric mean These findings 15 – NO2 levels µg/m3 indicate that reducing Indoor nitrogen dioxide NO ) exposure indoors (NO22 emitted from 11.4 10 – unflued gas heating. in is important improving Respiratory health of the respiratory health children. 05 – 7.4 of children with asthma. 0 INDOOR OUTDOOR
    • Adhesion of Streptococcus pneumoniae to human airway epithelial cells exposed to urban particulate matter Mushtaq JACI 2011;127:1236 Background Epidemiologic studies report an association between pneumonia and urban particulate matter (PM) less than 10 microns (μm) in aerodynamic diameter (PM10). Streptococcus pneumoniae is a common cause of bacterial pneumonia worldwide. To date, the mechanism whereby urban PM enhances vulnerability to S pneumoniae infection is unclear. Adhesion of S pneumoniae to host cells is a prerequisite for infection. Host-expressed proteins, including the receptor for platelet-activating factor (PAFR), are co-opted by S pneumoniae to adhere to lower airway epithelial cells.
    • Adhesion of Streptococcus pneumoniae to human airway epithelial cells exposed to urban particulate matter Mushtaq JACI 2011;127:1236 1) Cultured with PM10 and PM2.5 2) Then infected with S pneumoniae Airway epithelial cells A 549 PM10 and PM2.5 increased S pneumoniae adhesion
    • Adhesion of Streptococcus pneumoniae to human airway epithelial cells exposed to urban particulate matter Mushtaq JACI 2011;127:1236 1) Cultured with PM10 and PM2.5 2) Then infected with S pneumoniae Airway epithelial cells A 549 PM10 and PM2.5 increased S pneumoniae adhesion Adhesion was attenuated by N-acetyl cysteine antioxidant
    • Adhesion of Streptococcus pneumoniae to human airway epithelial cells exposed to urban particulate matter Mushtaq JACI 2011;127:1236 1) Cultured with PM10 and PM2.5 2) Then infected with S pneumoniae Airway epithelial cells A 549 PM10 and PM2.5 increased PM The ability of combustion to induce oxidative stress in S pneumoniae adhesion airway cells is considered to be an important factor in the initiation of adverse health Adhesion was attenuated effects. by N-acetyl cysteine antioxidant
    • Feather bedding and childhood asthma associated with house dust mite sensitisation: a randomised controlled trial. Glasgow Arch Dis Child 2011;96:541IntroductionObservational studies report inverse associations between the use offeather upper bedding (pillow and/or quilt) and asthma symptoms but thereis no randomised controlled trial evidence assessing the role of featherupper bedding as a secondary prevention measure.ObjectiveTo determine whether, among children not using feather upper bedding,a new feather pillow and feather quilt reduces asthma severity among housedust mite (HDM) sensitised children with asthma over a 1-year periodcompared with standard dust mite avoidance advice, and giving children a newmite-occlusive mattress cover.
    • Feather bedding and childhood asthma associated with house dust mite sensitisation: a randomised controlled trial. Glasgow Arch Dis Child 2011;96:541 % children with frequent wheeze 70 – (≥4 episodes) 197 children with HDM sensitisation and moderate 60 – 63.8% ns to severe asthma. 50 – 55.3% New upper bedding duck 40 – feather pillow and quilt and a mite-occlusive 30 – mattress cover (feather) 20 – Standard care and a mite- occlusive mattress cover 10 – (standard). 0 Feather Standard bedding care
    • Feather bedding and childhood asthma associated with house dust mite sensitisation: a randomised controlled trial. Glasgow Arch Dis Child 2011;96:541 197 children with HDM sensitisation and moderate % children with to severe asthma. speech-limiting wheeze New upper bedding duck feather pillow and quilt 30 – ns and a mite-occlusive 22.6% mattress cover (feather) 20 – 20.2% Standard care and a mite- 10 – occlusive mattress cover (standard). 0 Feather Standard bedding care
    • Feather bedding and childhood asthma associated with house dust mite sensitisation: a randomised controlled trial. Glasgow Arch Dis Child 2011;96:541 % children with sleep disturbed because of wheezing 197 children with HDM 60 – sensitisation and moderate ns to severe asthma. 50 – 55.3% New upper bedding duck 50.0% 40 – feather pillow and quilt and a mite-occlusive 30 – mattress cover (feather) 20 – Standard care and a mite- occlusive mattress cover 10 – (standard). 0 Feather Standard bedding care
    • Feather bedding and childhood asthma associated with house dust mite sensitisation: a randomised controlled trial. Glasgow Arch Dis Child 2011;96:541 % children with sleep disturbed because of wheezing 197 children with HDM 60 – sensitisation and moderate ns to severe asthmapillow No cover . 50 – 55.3% New upper bedding duck 50.0% or cover quilt feather pillow and quilt 40 – was provided. and a mite-occlusive 30 – mattress cover (feather) 20 – Standard care and a mite- occlusive mattress cover 10 – (standard). 0 Feather Standard bedding care
    • Feather bedding and childhood asthma associated with house dust mite sensitisation: a randomised controlled trial. Glasgow Arch Dis Child 2011;96:541 OR for frequent wheeze (≥4 episodes) The association of feather upper 2.0 – bedding use (pillow and quilt) and 1.5 – 1.88 respiratory outcomes, with 1.0 – further consideration 0.5 – of child‟s usual 0.61 sleeping position. 0 0 Non-supine Supine children children Feather bedding use
    • Feather bedding and childhood asthma associated with house dust mite sensitisation: a randomised controlled trial. Glasgow Arch Dis Child 2011;96:541 The association of feather upper OR for speech-limiting wheeze bedding use (pillow and quilt) and 1.5 – respiratory outcomes, with 1.0 – further consideration 0.5 – 0.90 of child‟s usual 0.0 sleeping position. 0 0 Non-supine Supine children children Feather bedding use
    • Feather bedding and childhood asthma associated with house dust mite sensitisation: a randomised controlled trial. Glasgow Arch Dis Child 2011;96:541 The association of feather upper OR for sleep disturbed because of wheezing (≥1 nights per week) bedding use (pillow and quilt) and 1.5 – respiratory outcomes, with 1.0 – further consideration 0.5 – of child‟s usual 0.57 0.0 sleeping position. 0 0 Non-supine Supine children children Feather bedding use
    • Feather bedding and childhood asthma associated with house dust mite sensitisation: a randomised controlled trial. Glasgow Arch Dis Child 2011;96:541 Intervention The association ofrisk reduced the feather upper being of sleep OR for sleep disturbed because of wheezing (≥1 nights per week) bedding use (pillow disturbed because and quilt) and of wheezing and 1.5 – respiratory wheeze to severe outcomes, witha 1.0 – further consideration greater extent for 0.5 – of child‟s usual slept children who 0.57 0.0 sleeping position. supine. 0 0 Non-supine Supine children children Feather bedding use
    • Influence of host & environmental factors on wheezing severity in infants: findings from the PARIS birth cohort. Herr, Clin Exp Allergy 2012;42:275 OR for recurrent wheezing 03 – Wheezing severity in infants aged 18 mo. 02 – in the PARIS birth cohort. Severe wheeze defined 1.62 1.50 as wheeze that required 01 – 1.39 inhaled corticosteroid and/or hospital-based care. p=0.008 p=0.068 p=0.003 00 Overweight Daily use Carpet covered of cleaning floor sprays
    • • pollution indoor • swimming pool
    • High-Dose Docosahexaenoic Acid Supplementation ofPreterm Infants: Respiratory and Allergy Outcomes Manley Pediatrics 2011;128:e71•Docosahexaenoic acid (DHA) is an n-3 long-chainpolyunsaturated fatty acid (LCPUFA), which along with theother n-3 LCPUFA, eicosapentaenoic acid, is provided in thediet by fish and fish oils.•These LCPUFA are known to modulate inflammation and arealso postulated to modulate the neonatal immune response.•For example, supplementation with n-3 LCPUFA duringpregnancy is known to be associated with decreasedmessenger RNA levels of TH2-related molecules in the fetusand decreased maternal inflammatory cytokines.
    • High-Dose Docosahexaenoic Acid Supplementation of Preterm Infants: Respiratory and Allergy Outcomes Manley Pediatrics 2011;128:e71 657 preterm infants 33 RR of BDP in boys weeks‟ gestation who consumed expressed breast 1.0 – milk from mothers taking 0.9 – either tuna oil 0.8 – 0.7 – (high-DHA diet) or soy oil (standard-DHA) capsules. 0.6 – 0.5 – 0.67 0.4 – Incidence of 0.3 – p=0.03 bronchopulmonary dysplasia 0.2 – 0.1 – (BPD) and parental reporting 0 of atopic conditions over the DHA diet first 18 months of life.
    • High-Dose Docosahexaenoic Acid Supplementation of Preterm Infants: Respiratory and Allergy Outcomes Manley Pediatrics 2011;128:e71 657 preterm infants 33 RR of BDP in all infants with weeks‟ gestation who a birth weight of 1250 g consumed expressed breast 1.0 – milk from mothers taking 0.9 – either tuna oil (high-DHA 0.8 – 0.75 0.7 – diet) or soy oil (standard- 0.6 – DHA) capsules. 0.5 – 0.4 – p=0.04 Incidence of 0.3 – bronchopulmonary dysplasia 0.2 – 0.1 – (BPD) and parental reporting 0 of atopic conditions over the DHA diet first 18 months of life.
    • High-Dose Docosahexaenoic Acid Supplementation of Preterm Infants: Respiratory and Allergy Outcomes Manley Pediatrics 2011;128:e71 657 preterm infants 33 RR of reported hay fever weeks‟ gestation who in all infants at either consumed expressed breast 12 or 18 months 1.0 – milk from mothers taking 0.9 – either tuna oil (high-DHA 0.8 – diet) or soy oil (standard- 0.7 – DHA) capsules. 0.6 – 0.5 – 0.4 – Incidence of bronchopulmonary dysplasia 0.3 – 0.2 – 0.41 (BPD) and parental reporting 0.1 – p=0.03 of atopic conditions over the 0 first 18 months of life. DHA diet
    • Folic Acid Use in Pregnancy and the Development of Atopy, Asthma, and Lung Function in Childhood Magdelijns Pediatrics 2011;128:e144 KOALA Birth Cohort •Maternal folic acid Study (n=2834). supplement use during Data on eczema pregnancy was not associated and wheeze at with increased risk of 3, 7, 12, and 24 wheeze, lung months, 4 function, asthma, or related to 5 years, and atopic outcomes in the 6 to 7 years. offspring. Intracellular folic acid •Maternal ICF level in late pregnancy was inversely (ICF) determined in blood samples taken at associated with asthma risk at ~35 weeks of pregnancy age 6 to 7 years in a dose- (n=837). dependent manner
    • Folic Acid Use in Pregnancy and the Development of Atopy, Asthma, and Lung Function in Childhood Magdelijns Pediatrics 2011;128:e144 KOALA Birth Cohort Our results do not •Maternal folic acid Study (n=2834). supplement use during confirm any meaningful association between folic Data on eczema pregnancy was not associated acid supplement use during and wheeze at with increased risk of wheeze, pregnancy and atopic 3, 7, 12, and 24 months, lung function, asthma, or 4diseases in the offspring. to 5 years, and related atopic outcomes in the 6 to 7 years. ICF levels Higher offspring. in pregnancy tended, •Maternal ICF level in late Intracellular folic acid at most, toward a small pregnancy was inversely (ICF) determined in decreased risk associated with asthma risk at blood samples taken at for developing ~35 weeksasthma. of pregnancy age 6 to 7 years in a dose- (n=837). dependent manner (p for trend =0.05).
    • Folic Acid Use in Pregnancy and the Development of Atopy, Asthma, and Lung Function in Childhood Magdelijns Pediatrics 2011;128:e144Prevalence of wheeze (A) and eczema (B) at different ages
    • Folic Acid Use in Pregnancy and the Development of Atopy, Asthma, and Lung Function in Childhood Magdelijns Pediatrics 2011;128:e144 OR for asthma at 6-7 yrs1.0 – 1.0 p<0.005 for trend 0.730.5 – 0.46 0.41 0.310.0 1st Quintile 2nd Quintile 3rd Quintile 4th Quintile 5th Quintile (≤ 480 nmol/L) (481–643 (644–862 (863–1139 (≥ 1140 nmol/L) nmol/L) nmol/L) nmol/L) Intracellular folic acid Levels (Divided Into Quintiles)
    • Pediatric Submersion Events in Portable Above-Ground Pools in the United States, 2001–2009 Shields Pediatrics 2011;128:45 Number of submersion events for children <12 yrs according to year and type of event (fatal, nonfatal, and overall) in the United States in 2001–2009 Fatal and nonfatal submersion events involving children younger than 12 yrs in portable pools from 2001 to 2009.
    • The relationship between maternal folate status in pregnancy, cord blood folate levels, and allergic outcomes in early childhood. Dunstan, Allergy 2012;67:50 Infant allergic outcomes at 1 yr of age according to maternal folic acid taken as a supplement in pregnancy. 628 women recruited in the last trimester of pregnancy. Folate status determined by: - food frequency questionnaires; - levels in maternal and cord blood serum. Infant allergic outcomes at 1 yr of age (n=484).
    • The relationship between maternal folate status in pregnancy, cord blood folate levels, and allergic outcomes in early childhood. Dunstan, Allergy 2012;67:50 Cord blood folate levels and allergic outcomes. 628 women recruited in the last trimester of pregnancy. Folate status determined by: - food frequency questionnaires; - levels in maternal and cord blood serum. Infant allergic outcomes at 1 yr of age (n=484).
    • The relationship between maternal folate status in pregnancy, cord blood folate levels, and allergic outcomes in early childhood. Dunstan, Allergy 2012;67:50 Cord blood folate levels and allergic There was a nonlinear outcomes. relationship between 628 women recruited in cord blood folate the last trimester and sensitization, of pregnancy. levels with folate <50 nmol/L Folate status p=0.024) (OR=3.02, determined by: and >75 nmol/L - food frequency (OR=3.59, p=0.008) questionnaires; greater associated with sensitization risk - levels in maternal and cord blood serum. 50 than levels between and 75 nmol/L. Infant allergic outcomes at 1 yr of age (n=484).
    • The relationship between maternal folate status in pregnancy, cord blood folate levels, and allergic outcomes in early childhood. Dunstan, Allergy 2012;67:50 In utero folate status in infants who developed subsequent eczema 628 women recruited in vs the last trimester those who did not. of pregnancy. Folate status determined by: - food frequency (μg/d) questionnaires; - levels in maternal and cord blood serum. Infant allergic outcomes at 1 yr of age (n=484). DFE=dietary folate equivalent units
    • The relationship between maternal folate status in pregnancy, cord blood folate levels, and allergic outcomes in early childhood. Dunstan, Allergy 2012;67:50 In utero folate status Although maternal in infants who developed subsequent eczema 628 women recruited in folate intake from vs the last trimester those who did not. foods was also not of pregnancy. different, folate Folate status determined derived from by: supplements was - food frequency (μg/d) higher (p=0,017) in questionnaires; children with - levels in maternal and subsequent eczema. cord blood serum. Infant allergic outcomes at 1 yr of age (n=484). DFE=dietary folate equivalent units
    • The relationship between maternal folate status in pregnancy, cord blood folate levels, and allergic outcomes in early childhood. Dunstan, Allergy 2012;67:50 In utero folate status Infants exposed to in infants who developed subsequent eczema 628 >500 μg folic in women recruited vs the acid/day as a last trimester those who did not. of pregnancy. supplement in utero were more likely Folate status determined by: develop eczema to - food frequency (μg/d) than those taking questionnaires; <200 μg/day - levels in maternal and cord blood p=0.013). (OR=1.85, serum. Infant allergic outcomes at 1 yr of age (n=484). DFE=dietary folate equivalent units
    • Cord blood T-regs with stable FOXP3 expression are influenced by prenatal environment & associated with atopic dermatitis at the age of 1 yr. Hinz, Allergy 2012;67:380 OR for atopic dermatitis during the 1°yr of life Blood samples from pregnant women 2 – (34th gestational week) & in cord blood 1.55 (n=346 mother-child pairs). 1 – T-reg numbers detected via DNA demethylation in the FOXP3. in children with lower 0 T-reg numbers at birth.
    • Cord blood T-regs with stable FOXP3 expression areinfluenced by prenatal environment & associated with atopic dermatitis at the age of 1 yr. Hinz, Allergy 2012;67:380 % T-reg cell in cord blood1.4 - p=0.0421.2 - 1.38% p=0.0391.1 - 1.17%0.8 - 1.05% 0.85%0.6 -0.4 -0.2 -0 NEVER DAILY NO YES Usage of disinfectants Maternal smoking/environmental tobacco smoke exposure at home
    • Gene polymorphisms, breast-feeding and development of food sensitization in early childhood Hong JACI 2011;128:374BackgroundThe effect of breast-feeding of development of allergic diseaseis uncertain. There are no data that show whether thisrelationship varies by individual genotypes.ObjectivesWe sought to evaluate the effect of breast-feedingand gene-breast-feeding interactions on food sensitization (FS)in a prospective US birth cohort.
    • Gene polymorphisms, breast-feeding and development of food sensitization in early childhood Hong JACI 2011;128:374 HR for food sensitization 2 – (sIgE≥ 0.35KUA/L) 970 children prospectively followed since birth. Breast-feeding history. Specific IgE level 1 – 1.5 of ≥ 0.35kUA/L to any of 8 common food allergens. 0 88 potentially functional single Children who were ever nucleotide polymorphisms (SNPs) genotyped from breast-fed (n=739), including 18 genes involved in innate exclusively breast-fed immunity or TH1/TH2 balance. children, compared with never breast-fed children (n=231).
    • Gene polymorphisms, breast-feeding and development of food sensitization in early childhood Hong JACI 2011;128:374 This association HR for food sensitization was significantly modified 2 – (sIgE≥ 0.35KUA/L) by rs425648 in the IL-12 receptor ß1 gene 970 children prospectively (IL12RB1; p for interaction followed since birth. =0.0007): Breast-feeding history. breast-feeding increased Specific IgE level FS 1 – 1.5 the risk of (HR, 0.35kUA/L to any of of ≥ 2.0; 95% CI, 1.4-3.1;p=80.0005) food allergens. common in children carrying 0 the GG genotype 88 potentially functional single Children who were ever nucleotide polymorphisms but decreased the risk breast-fed (n=739), including (HR, 0.6; 95% CI,from (SNPs) genotyped 0.3-1.4; exclusively breast-fed 18 genes p= 0.252) innate involved in immunity or TH1/TH2 balance. in children carrying the children, compared with never GT/TT genotype. breast-fed children (n=231).
    • Gene polymorphisms, breast-feeding and development of food sensitization in early childhood Hong JACI 2011;128:374 HR for food sensitization 2 – (sIgE≥ 0.35KUA/L) 970 childreninteractions Similar prospectively followed since birth. 1.5 were observed for Single Breast-feeding history.Nucleotide Polymorphisms 1 – Specific the level in IgE Toll-like receptor 9 of ≥ 0.35kUA/L to any of 8 common food allergens. (TLR9; rs352140) 0 88 and thymic stromal potentially functional single Children who were ever nucleotide polymorphisms lymphopoietin (SNPs) genotyped from breast-fed (n=739), including (TSLP; rs3806933) exclusively breast-fed 18 genes involved in innate genes. immunity or T 1/T 2 balance. children, compared with never H H breast-fed children (n=231).
    • Gene polymorphisms, breast-feeding and development of food sensitization in early childhood Hong JACI 2011;128:374 HR for food sensitization 2 – (sIgE≥ 0.35KUA/L) The effects 970 children prospectively on of breast-feeding followed sinceSensitization Food birth. Breast-feeding history. by was modified Single Nucleotide Specific IgE level 1 – 1.5 Polymorphisms of ≥ 0.35kUA/L to any of 8 common food allergens. in the 0 IL12RB1, TRL9 and TSLP 88 potentially functional single Children who were ever nucleotide polymorphisms genes both individually (SNPs) genotyped from breast-fed (n=739), including and jointly. exclusively breast-fed 18 genes involved in innate immunity or TH1/TH2 balance. children, compared with never breast-fed children (n=231).
    • FADS gene cluster modulates the effect of breastfeeding on asthma. Results from the GINIplus and LISAplus studies. Standl, Allergy 2012;67:831. Breastfeeding (BF) is widely recognized to have beneficial effects on asthma and atopy, although not all results are conclusive.2. Among other factors in breast milk, the composition of polyunsaturated fatty acids (PUFA) of breast milk has been proposed to cause the protective effect.3. Linoleic acid (LA, 18:2n-6), the most common dietary n-6 PUFA, is metabolized to arachidonic acid (AA, 20:4n-6). Arachidonic acid can act as substrate of inflammatory eicosanoids.
    • FADS gene cluster modulates the effect of breastfeeding on asthma. Results from the GINIplus and LISAplus studies. Standl, Allergy 2012;67:834. Eicosapentaenoic acid (EPA, 20:5n-3) and docosahexaenoic acid (DHA, 22:6n-3), products of the metabolism of the essential n-3 fatty acid α-linolenic acid (ALA, 18:3n-3), have been suggested to have beneficial effects on allergic inflammation.5. This led to the hypothesis that n-6 PUFA intake may enhance the development of allergic diseases in susceptible individuals. In contrast, n-3 PUFA are suggested to have protective effects against allergic diseases.6. The fatty acid desaturase 1 and 2 genes (FADS1 and FADS2) encode the enzymes delta-5-desaturase and delta-6- desaturase, respectively, which regulate the conversion of the precursor essential fatty acids to long chain metabolites.
    • FADS gene cluster modulates the effect of breastfeeding on asthma. Results from the GINIplus and LISAplus studies. Standl, Allergy 2012;67:83 Asthma prevalence stratified by FADS genotype and breastfeeding (1:major allele, 2:minor allele). 2 German prospective birth cohort studies (n=2245). BF during the first 6 mo. Asthma by age 10 yrs.
    • FADS gene cluster modulates the effect ofbreastfeeding on asthma. Results from the GINIplus and LISAplus studies. Standl, Allergy 2012;67:83 Results of logistics regression models of breastfeeding (BF) on asthma stratified by genotype.
    • FADS gene cluster modulates the effect ofbreastfeeding on asthma. Results from the GINIplus and LISAplus studies. Standl, Allergy 2012;67:83 Results of logistics regression models of breastfeeding (BF) on asthma stratified by genotype. Minor allele carriers have a lower proportion of products of the fatty acid metabolism and therefore a lower proportion of AA, a product of the n-6 pathway which may reduce the risk of asthma.
    • FADS gene cluster modulates the effect ofbreastfeeding on asthma. Results from the GINIplus and LISAplus studies. Standl, Allergy 2012;67:83 Results of logistics regression models of breastfeeding (BF) on asthma stratified by genotype. The association between exclusive BF and asthma is modified by the genetic variants of FADS genotypes in children.
    • • protective factors for atopic diseases:-diet
    • Tomato juice protects the lungs of the offspring offemale rats exposed to nicotine during gestation and lactation. Maritz Pediatr Pulmonol 2011;46:976 Maternal nicotine exposure during pregnancy and lactation Structural changes started to appear around postnatal day 42, that is, 3 weeks after weaning and thus the onset of nicotine withdrawal. Structural integrity of the lungs of the offspring
    • Tomato juice protects the lungs of the offspring offemale rats exposed to nicotine during gestation and lactation. Maritz Pediatr Pulmonol 2011;46:976 Maternal nicotine exposure during pregnancy and lactation Rich source of antioxidants such as lycopene, will prevent Structural changes the effects of started to appear around nicotine on the lungs postnatal day 42, that is, of the offspring. 3 weeks after weaning and thus the onset of nicotine withdrawal. Structural integrity of the lungs of the offspring
    • Tomato juice protects the lungs of the offspring offemale rats exposed to nicotine during gestation and lactation. Maritz Pediatr Pulmonol 2011;46:976 Maternal nicotine exposure during pregnancy and lactation All these nicotine- induced structural changes were Structural changes prevented by started to appear around supplementing the postnatal day 42, that is, mothers diet with 3 weeks after weaning tomato juice and thus the onset of nicotine withdrawal. Structural integrity of the lungs of the offspring
    • Tomato juice protects the lungs of the offspring offemale rats exposed to nicotine during gestation and lactation. Maritz Pediatr Pulmonol 2011;46:976 Nicotine + tomato juice Nicotine. Arrows = emphysema
    • Allergic disease in infants up to 2 years of age in relation toplasma omega-3 fatty acids and maternal fish oil supplementationin pregnancy and lactation. Furuhjelm Pediatr Allergy Immunol 2011;22:505 % children with IgE Maternal omega-3 long-chain associated diseases polyunsaturated fatty acids 30 – (ω-3 LCPUFA) supplementation in pregnancy and lactation. 25 – 30% P=0.01 145 pregnant women. 20 – Daily supplementation with 1.6 g eicosapentaenoic acid 15 – 13% (EPA) and 10 – 1.1 g docosahexaenoic acid (DHA) or placebo starting in 05 – the 25th gestational week 00 and continuing through ω-3 placebo 3.5 months of breastfeeding. supplemented
    • Allergic disease in infants up to 2 years of age in relation toplasma omega-3 fatty acids and maternal fish oil supplementationin pregnancy and lactation. Furuhjelm Pediatr Allergy Immunol 2011;22:505 % children with IgE Maternal omega-3 long-chain associated diseases high proportions of polyunsaturated fatty acids 30 – DHA and EPA in (ω-3 LCPUFA) supplementation maternal and infant in pregnancy and lactation. 25 – 30% P=0.01 145plasma phospholipids pregnant women. 20 – were associated with Daily supplementation with less IgE-associated 1.6 g eicosapentaenoic acid 15 – 13% (EPA) and and a reduced disease 10 – 1.1 g docosahexaenoic allergic severity of the acid (DHA) or phenotype. placebo starting in 05 – the 25th gestational week 00 and continuing through ω-3 placebo 3.5 months of breastfeeding. supplemented
    • Allergic disease in infants up to 2 years of age in relation toplasma omega-3 fatty acids and maternal fish oil supplementationin pregnancy and lactation. Furuhjelm Pediatr Allergy Immunol 2011;22:505 % children with IgE Maternal omega-3 long-chain associated diseases polyunsaturated fatty acids DHA and EPA may act 30 – (ω-3through several anti- LCPUFA) supplementation in inflammatory mechanisms. pregnancy and lactation. 25 – 30% They inhibit the expression P=0.01 145 pregnant women. 20 – of inflammatory genes Daily supplementation withetc) (COX-2, IL-1α, 5-LOX 1.6 and adhesion molecules, g eicosapentaenoic acid 15 – 13% (EPA) and influence the antigen 10 – 1.1 g docosahexaenoicreduce presenting cells, acid (DHA) or placebo starting in 05 – lymphocyte proliferation and the 25th gestational week alter cytokine production. 00 and continuing through ω-3 placebo 3.5 months of breastfeeding. supplemented
    • Allergic diseases among very preterm infants according to nutrition after hospital discharge Zachariassen Pediatr Allergy Immunol 2011;22:515 A cow‟s milk-based human milk fortifier (HMF) added to mother‟s milk while breastfeeding or a •No difference was found cow‟s milk-based preterm between nutrition groups. formula compared to exclusively mother‟s milk •None developed food after hospital discharge. allergy. 324 VPI (gestational age 24–32 wk). Intervention period until 4 months corrected age (CA).
    • FADS gene variants modulate the effect of dietary fatty acid intake on allergic diseases in children Standl CEA 2011;41:17571. The association between dietary fatty acid intake and the development of atopic diseases has been inconsistent. This could be due to inter-individual genetic differences in fatty acid metabolism.2. n-3 PUFA can competitively inhibit the production of pro-inflammatory AA. This led to the hypothesis that n-6 PUFA intake may enhance the development of allergic diseases in susceptible individuals, mediated at least partly through an increase in IgE synthesis. In contrast, n-3 PUFA is suggested to have protective effects against allergic diseases.
    • FADS gene variants modulate the effect of dietary fatty acid intake on allergic diseases in children Standl CEA 2011;41:17573. The genes fatty acid desaturase 1 and 2 (FADS1 and FADS2) encode the enzymes delta-5-desaturase and delta-6-desaturase, respectively, which are involved in the fatty acid metabolic pathway.4. Daily margarine intake was significantly associated with asthma in individuals carrying the homozygous major allele.
    • Childhood diet and asthma and atopy at 8 years of age: the PIAMA birth cohort study Willers ERJ 2011;37:1060 OR for asthma symptoms in children with fruit PIAMA birth cohort. consumption at early age n=4146 1.0 – Associations between 0.93 food intake at early (2-3 yrs) and 0.5 – later (7-8 yrs) age. Asthma and atopy at 8 yrs of age. 0 per 1 consumption day per week
    • Childhood diet and asthma and atopy at 8 years of age: the PIAMA birth cohort study Willers ERJ 2011;37:1060 OR for asthma symptoms in children with fruit PIAMA birth cohort. consumption at early age n=4146 1.0 – Associations between 0.93 food intake at early (2-3 yrs) and 0.5 – later (7-8 yrs) age. Asthma and atopy at 8 yrs of age. 0 Prevention and per 1 consumption day Incidence of Asthma per week and Mite Allergy
    • Childhood diet and asthma and atopy at 8 years of age: the PIAMA birth cohort study Willers ERJ 2011;37:1060 In children with long term fruit PIAMA birth cohort. intake OR for 1.0 – n=4146 Associations between food intake 0.90 0.90 0.5 – at early (2-3 yrs) and later (7-8 yrs) age. Asthma and atopy 0 at 8 yrs of age. Asthma Sensitisation symptoms to inhaled allergens
    • Childhood diet and asthma and atopy at 8 years of age: the PIAMA birth cohort study Willers ERJ 2011;37:1060 In children with long term fruit PIAMA birth cohort. This study indicates intake OR for no consistent effects n=4146 1.0 – of increased early Associations between or late consumption, food intake 0.90 0.90 or long-term intake 0.5 – at early certain foods of (2-3 yrs) and later (7-8 yrs)and atopy on asthma age. in 8-yr-olds, Asthma and atopy 0 at 8 yrs of a possible with age. Asthma Sensitisation exception for fruit. symptoms to inhaled allergens
    • Dietary antioxidants and forced expiratory volumein 1 s decline: the Health, Aging and Body Composition study Bentley, Eur Respir J 2012;39:979 1) Ageing has been described as the accumulation of oxidative damage that is incompletely repaired by the body‟s antioxidant defences. 2) This damage is caused by free radicals produced in the body via normal metabolic processes and inflammation, and by exogenous free radicals, such as from smoking and noxious gases. 3) In the lungs, ageing is associated with declining lung function, and rate of decline increases with advancing age.
    • Dietary antioxidants and forced expiratory volumein 1 s decline: the Health, Aging and Body Composition study Bentley, Eur Respir J 2012;39:979 In continuing smokers higher intake of fruit and vegetables were associated with a slower rate of FEV1decline compared with a lower intake 1,443 participants 0 – completed a food frequency questionnaire. p=0.003 -10 – Self-reported smoking history. + FEV1 at both baseline -20 – and after 4 yrs of -24mL/yr followup. -30 -
    • Dietary antioxidants and forced expiratory volumein 1 s decline: the Health, Aging and Body Composition study Bentley, Eur Respir J 2012;39:979 In continuing smokers higher intake of fruit and In quitters vegetables were associated with a slower rate (a current smoker at of FEV1decline compared with a lower intake study participants had 1,443 baseline who 0 – completed a food quit during follow-up), frequency questionnaire. higher intake was p=0.003 associated with an -10 – Self-reportedrate of attenuated smoking history. decline for each + nutrient studied -20 – FEV(1p≤0.003 for all at both baseline and after 4 yrs of -24mL/yr models). followup. -30 -
    • Dietary antioxidants and forced expiratory volumein 1 s decline: the Health, Aging and Body Composition study Bentley, Eur Respir J 2012;39:979 In continuing smokers higher intake of fruit and vegetables were associated with a slower rate of FEV1decline compared with a lower intake 1,443 participants In nonsmoking 0 – completed a food participants, frequency questionnaire. there was little or p=0.003 no association Self-reported -10 – smoking history.rate of diet and + of decline FEV1 at both baseline -20 – in FEV1. -24mL/yr and after 4 yrs of followup. -30 -
    • Dietary antioxidants and forced expiratory volume in 1 s decline: the Health, Aging and Body Composition study Bentley, Eur Respir J 2012;39:979 In continuing smokers higher intake of fruit and The intake of vegetables were associated with a slower rate of FEV1decline compared with a lower intake nutrients with 1,443 participants 0 – completed a food antioxidant frequency questionnaire. properties may p=0.003modulate lung function Self-reported -10 – decline in older smoking history. adults exposed to + FEV1 at bothsmoke. -20 – cigarette baseline -24mL/yr and after 4 yrs of followup. -30 -
    • Dietary factors and lung function in the general population: wine and resveratrol intake Siedlinski M , Eur Respir J 2012;39:385ABSTRACT: Wine intake is associated with a better lung functionin the general population, yet the source of this effect is unknown.Resveratrol, a polyphenol in wine, has anti-inflammatory propertiesin the lung, its effects being partially mediated via induction ofSirtuin (SIRT)1 activity.We assessed the impact of wine and resveratrol intake, andSIRT1 single-nucleotide polymorphisms (SNPs) on lungfunction in the general population.
    • Dietary factors and lung function in the general population: wine and resveratrol intake Siedlinski M , Eur Respir J 2012;39:385 • Resveratrol intake was Effects of red and associated with white wine and higher FVC levels. resveratrol intake. FEV1, FVC and FEV1/FVC. • White wine intake with Population-based cohort higher FEV1 levels and (n=3,224). lower risk of airway obstruction.
    • Dietary factors and lung function in the general population: wine and resveratrol intake Siedlinski M , Eur Respir J 2012;39:385 Mean adjusted FEV1 and FVC for the subjects according tothe average intake of white wine and total resveratrol FEV1 white FEV1 total resveratrol wine FVC white wine FVC total resveratrol
    • Dietary factors and lung function in the general population: wine and resveratrol intake Siedlinski M , Eur Respir J 2012;39:385 Mean adjusted FEV1 and FVC for the subjects according to Polyphenolicthe average intake of white wine and total compounds present in white resveratrol wine may exert beneficial FEV1 total resveratrol FEV1 white effects on lung function. wine Plausible candidates in this respect are tyrosol and hydroxytyrosol, polyphenolic white total molecules that, FVC wine resveratrol FVC white wine similar to resveratrol, exhibit antioxidant and cardioprotective effects
    • Dietary factors and lung function in the general population: wine and resveratrol intake Siedlinski M , Eur Respir J 2012;39:385 Mean adjusted FEV1 and FVC for the subjects according tothe average intake The white wine and total of positive resveratrol we observed between association FEV1 white white FEV1 total resveratrol wine intake and higher wine FEV1 reflects a very modest average consumption of 1.0–1.5 glasses of white wine per week (i.e. 7.4 g·day-1) and, thus, we FVC white wine by no meanstotal to suggest that FVC aim resveratrol more than moderate white wine drinking could be considered as beneficial health behaviour.
    • Dietary factors and lung function in the general population: wine and resveratrol intake Siedlinski M , Eur Respir J 2012;39:385Beneficial effects of wine consumption are postulated to account for the„„French paradox‟‟, the observation of lower mortality due to coronaryheart disease in the French population despite thispopulation‟s relatively high consumption of a cholesterol- andsaturated fat-rich diet.The proposed mechanism includes the inhibition of platelet reactivity bywine and resveratrol is a prominent candidate responsible for the vascularprotection provided by wine.However, our study shows that white wine intake and not redwine intake,the major dietary resveratrol source, is associated with a lower risk ofairway obstruction and with higher FEV1, both of which are indices ofCOPD.This is of great importance given the fact that reduced lung function is amarker for cardiovascular-related mortality.
    • Fruit and vegetable consumption in relation to allergy: Disease-related modification of consumption? Rosenlund JACI 2011;127:1219 Cross-sectional data from OR for Rhinitis a Swedish birth cohort. 1.0 – Fruit and vegetable consumption. 0.5 – 0.62 Allergic diseases by parental questionnaires p=0.002 0.0 at the 8-year follow-up. Total fruit (highest vs lowest quartile)
    • Fruit and vegetable consumption in relation to allergy: Disease-related modification of consumption? Rosenlund JACI 2011;127:1219 Cross-sectional data from OR for Rhinitis a Swedish birth cohort. Whereas no 1.0 – association was Fruit and vegetable observed for consumption. total vegetable 0.5 – 0.62 Allergic diseases by intake. parental questionnaires p=0.002 0.0 at the 8-year follow-up. Total fruit (highest vs lowest quartile)
    • Fruit and vegetable consumption in relation to allergy: Disease-related modification of consumption? Rosenlund JACI 2011;127:1219 Cross-sectional data from OR for Rhinitis a Swedish birth of Intake cohort. 1.0 – apples/pears and carrots was Fruit and vegetable consumption. associated inversely with 0.5 – 0.62 Allergic diseases by an rhinitis, asthma, parental questionnaires p=0.002 d atopic 0.0 at the sensitization. 8-year follow-up. Total fruit (highest vs lowest quartile)
    • Fruit and vegetable consumption in relation to allergy: Disease-related modification of consumption? Rosenlund JACI 2011;127:1219 50% of the children with Cross-sectional data from rhinitis were sensitized OR for Rhinitis a Swedish birch pollen, which against birth cohort. 1.0 – may cross-react with apples Fruit and and carrots. vegetable After exclusion of children consumption. food-related who reported allergic symptoms, most of 0.5 – 0.62 Allergic diseases by the observed inverse parental questionnaires p=0.002 associations moved toward 0.0 at the the null and became 8-year follow-up. Total fruit nonsignificant. (highest vs lowest quartile)
    • Selenium status and allergic disease in a cohort of New Zealand children. Thomson, Clin Exp Allergy 2012;42:560 The New Zealand Asthma and Allergy Cohort Study, Selenium is essential a prospective birth cohort . for the optimal functioning of the selenoenzymes 1105 infants born glutathione peroxidases (GPx) 1997-2001. and thioredoxin reductases, 6-yr assessment (n=635). powerful antioxidants, and is found abundantly Plasma selenium (PlSe) in lung tissue and whole blood glutathione and the extracellular fluid peroxidase activity (WBGPx). of the respiratory system.
    • Selenium status and allergic disease in a cohort of New Zealand children. Thomson, Clin Exp Allergy 2012;42:560 OR for persistent wheeze The New Zealand Asthma at 6 yrs 03 – and Allergy Cohort Study, a prospective birth cohort. p=0.09 for trend 1105 infants born 02 – 2.04 1997-2001. 6-yr assessment (n=635). 1.34 01 – Plasma selenium (PlSe) 0.95 1 and whole blood glutathione peroxidase 00 activity (WBGPx). 1 2 3 4 Quartiles of blood glutathione peroxidase activity
    • Vitamin D
    • Umbilical cord plasma 25-hydroxyvitamin D concentration and immune function at birth: the Urban Environment and Childhood Asthma study Chi CEA 2011;41:842 Relationship between time of year 568 newborns, and vitamin D levels. 520 of whom had at least one atopic parent. Umbilical cord (UC) 25-hydroxyvitamin D and the cytokine responses of UC blood mononuclear cells.
    • Umbilical cord plasma 25-hydroxyvitamin D concentration and immune function at birth: the Urban Environment and Childhood Asthma study Chi CEA 2011;41:842  The 25th, 50th, and 75th 568 newborns, percentiles of UC plasma 25(OH) 520 of whom had at D level were 15.0, 20.2, and least one atopic 25.6 ng/mL, respectively. parent.  IFN-γ release after LPS Umbilical cord (UC) stimulation was weakly positively 25-hydroxyvitamin D correlated with UC 25(OH)D and the cytokine concentration (r=0.11, P=0.01). responses of UC  UC plasma 25(OH)D concentration blood mononuclear was inversely related to the cells. number of CD25+FoxP3 (r=−0.29, P=0.06) cells.
    • Umbilical cord plasma 25-hydroxyvitamin D concentration and immune function at birth: the Urban Environment and Childhood Asthma study Chi CEA 2011;41:842  The 25th, 50th, and 75th 568 newborns, higher vitamin D levels percentiles of UC plasma 25(OH) 520 of at birth may be whom had at D level were 15.0, 20.2, and least one atopic associated with a lower 25.6 ng/mL, respectively. parent. number of  IFN-γ release after LPS T-regulatory cells. stimulation was weakly positively Umbilical cord (UC) Vitamin D status in correlated with UC 25(OH)D 25-hydroxyvitamin D utero may influence concentration (r=0.11, P=0.01). and the cytokine immune regulation in  UC plasma 25(OH)D concentration responses of UC early life. was inversely related to the blood mononuclear cells. number of CD25+FoxP3 (r=−0.29, P=0.06) cells.
    • Umbilical cord plasma 25-hydroxyvitamin Dconcentration and immune function at birth: the Urban Environment and Childhood Asthma study Chi CEA 2011;41:842 Correlations between umbilical cord plasma 25(OH)D concentration and umbilical cord mononuclear cell characteristics related to T-regulatory cells among URECA study newborns in born in the Boston site
    • The role of vitamin D in the immunopathogenesisof allergic skin diseases. Benson, Allergy 2012;67:296 1) Vitamin D deficiency: serum 25(OH)D <10ng/ml; 2) Vitamin D insufficiency: serum 25(OH)D 21-29 ng/ml; 3) Low Vitamin D levels connected with: - higher cardiovascular mortality; - increased risk of cancer; - increased risk of Diabetes Mellitus; - increased risk of infections.
    • The role of vitamin D in the immunopathogenesisof allergic skin diseases. Benson, Allergy 2012;67:296 Metabolism of Vitamin D3
    • The role of vitamin D in the immunopathogenesis of allergic skin diseases. Benson, Allergy 2012;67:296• Conflicting data surrounding the effect that Vitamin D has on the development of allergic skin diseases: - several studies collectively support the theory that increased Vitamin D may be tied to allergic diseases, including atopic dermatitis; - several studies suggest that Vitamin D deficiency contributes to the development of atopic dermatitis; - several studies link Vitamin D supplementation with either the decreased risk or clinical improvment of atopic dermatitis.
    • The role of vitamin D in the immunopathogenesis of allergic skin diseases. Benson, Allergy 2012;67:296Studies assessing a link between allergic skin diseases & Vitamin D
    • The role of vitamin D in the immunopathogenesis of allergic skin diseases. Benson, Allergy 2012;67:296Studies assessing a link between allergic skin diseases & Vitamin D There is increasing evidence to show that vitamin D plays a significant role in the immune system, and specifically in allergic diseases. It is difficult to completely assess the role that vitamin D plays and large and prospective studies need to be conducted. Randomized controlled trials regarding treatment with vitamin D in the context of allergic diseases may also assist in determining a definitive link.
    • Circulating levels of 25-hydroxyvitamin D and humancathelicidin in healthy adults. Bhan JACI 2011;127:1302 Cathelicidins are a class of widely conserved antimicrobial peptides produced by essentially all mammalian species as part of the innate immune system. They have broad activity against both gram-positive and gram-negative bacteria and have additional effects, including neutralizing LPS, stimulating leukocyte chemotaxis, and promoting angiogenesis. Impairment in cathelicidin or other antimicrobial peptides has been linked to increased susceptibility to and severity of infection.
    • Circulating levels of 25-hydroxyvitamin D and human cathelicidin in healthy adults. Bhan JACI 2011;127:1302 Change in cathelicidin level by Plasma cathelicidin levels, change in 25(OH)D level after vitamin D status, and ergocalciferol treatment (n = 25) vitamin D supplementation. 60 healthy volunteers. Subjects with plasma 25(OH)D levels of ≤32 ng/mL were treated with ergocalciferol, 50,000 IU every other day, for 5 days. Posttreatment levels of 25(OH)D, cathelicidin 10 days after completing treatment.
    • Gene-vitamin D interactions on food sensitization: a prospective birth cohort study Liu, Allergy 2011;66:1442 % children with 649 children enrolled at birth; 50 – Vitamin D deficiency as cord blood 25(OH)D < 11 ng/ml; 40 – 44% Food sensitization: 30 – 37% sIgE ≥ 0.35 kUA/l to any of 8 common food allergens; 20 – Single-nucleotide polymorphisms (SNPs) in 11 10 – genes known to be involved in regulating IgE and 25(OH)D 0 concentrations. Vitamin D deficiency Food sensitization
    • Gene-vitamin D interactions on food sensitization: a prospective birth cohort study Liu, Allergy 2011;66:1442 649 children enrolled at OR for food sensitization in birth; children with vitamin D Vitamin D deficiency as cord deficiency blood 25(OH)D < 11 ng/ml; 2 – Food sensitization: sIgE ≥ 0.35 kUA/l to any 1.79 of 8 common food allergens; 1 – Single-nucleotide polymorphisms (SNPs) in 11 genes known to be involved in 0 regulating IgE and 25(OH)D concentrations. IL4 gene polymorphism (rs2243250) CC/CT genotypes
    • Gene-vitamin D interactions on food sensitization: a prospective birth cohort study Liu, Allergy 2011;66:1442 649 children enrolled at OR for food sensitization in birth; children with vitamin D Similar but weaker Vitamin D deficiency as cord deficiency interactions were blood 25(OH)D < 11 ng/ml; observed for SNPs 2 – in MS4 A2 Food sensitization: sIgE ≥ 0.35 kUA/l to any (rs512555), FCERIG 1.79 of 8 (rs2070901), and common food allergens; 1 – CYP24A1 Single-nucleotide (rs2762934). polymorphisms (SNPs) in 11 genes known to be involved in 0 regulating IgE and 25(OH)D concentrations. IL4 gene polymorphism (rs2243250) CC/CT genotypes
    • Gene-vitamin D interactions on food sensitization: a prospective birth cohort study Liu, Allergy 2011;66:1442 649 children enrolled at OR for food sensitization in birth; children with vitamin D Vitamin D all four SNPs When deficiency as cord deficiency blood 25(OH)D < 11 ng/ml; were simultaneously 2 – Food sensitization:strong considered, a gene-VSS interaction sIgE ≥ 0.35 kUA/l to any 1.79 of 8 commonevident was food allergens; 1 – (pinteraction =9x10-6) Single-nucleotide polymorphisms (SNPs) in 11 genes known to be involved in 0 regulating IgE and 25(OH)D concentrations. IL4 gene polymorphism (rs2243250) CC/CT genotypes
    • Relationship of 25-hydroxyvitamin D and asthma control in children Lewis, Ann Allergy Asthma Immunol 2012;108:281  Asthma prevalence and vitamin D deficiency rates have increased in parallel. It is accepted that serum 25-hydroxyvitamin D (25[OH]D) levels: ‹10-12 ng/mL represent deficiency, ‹20 ng/mL represent insufficiency, ›30 ng/mL represent sufficiency. A review of existing studies reveals associations between airway diseases and serum 25(OH)D using only a single measurement, and there are no dose-response data on the therapeutic effects of varying vitamin D levels in asthma.
    • Relationship of 25-hydroxyvitamin D and asthma control in children Lewis, Ann Allergy Asthma Immunol 2012;108:281 Effects of season and 20 patients, 6-17 years with vitamin D supplementation on physician diagnosis of chronic 25[OH]D ng/mL persistent asthma and current daily controller asthma medication.  Vitamina D supplement  Placebo Placebo or 1,000 IU of vitamin D daily. At initial (winter), 6-month (summer) and 1-year (winter) Visits, BMI, ACT score, spirometry, and serum 25(OH)D levels. Baseline 6 month 1 year winter summer winter
    • Relationship of 25-hydroxyvitamin D and asthma control in children Lewis, Ann Allergy Asthma Immunol 2012;108:281 Effects of season and 20 patients, 6-17 years with vitamin D supplementation on At the 6-month physician diagnosis of chronic 25[OH]D ng/mL persistent asthma and follow-up, the serum current daily controller 25(OH)D levels in asthma medication.  Vitamina D supplement both groups had  Placebo Placebo or increased vitamin D daily. 1,000 IU of significantly from baseline but did At initial (winter), 6-month not differ (summer) and 1-year (winter) significantly from Visits,eachACT score, BMI, other. spirometry, and serum 25(OH)D levels. Baseline 6 month 1 year winter summer winter
    • Relationship of 25-hydroxyvitamin D and asthma control in children Lewis, Ann Allergy Asthma Immunol 2012;108:281 Effects of season and 20 patients, 6-17 years with vitamin D supplementation on Only physician diagnosis of chronic 25[OH]D ng/mL persistent asthma and current of those in the 33% daily controller asthma medication. group supplemented  Vitamina D supplement  Placebo and 41.7% of those Placebo or 1,000 IU of vitamin D group in the placebo daily. were vitamin D At initial (winter), 6-month sufficient (summer) and 1-year (winter) at 6 months. Visits, BMI, ACT score, spirometry, and serum 25(OH)D levels. Baseline 6 month 1 year winter summer winter
    • Relationship of 25-hydroxyvitamin D and asthma control in children Lewis, Ann Allergy Asthma Immunol 2012;108:281 Effects of season and 20 patients, 6-17 years with vitamin D supplementation on physician diagnosis of chronic At 1-year 25[OH]D ng/mL persistent asthma and follow-up (winter), current daily controller asthma medication. 50% of those in the  Vitamina D supplement  Placebo supplemented group Placebo or and 20% vitamin D daily. 1,000 IU of of those in the placebo group At initial (winter), 6-month had sufficient (summer) and 1-year (winter) 25(OH)D levels. Visits, BMI, ACT score, spirometry, and serum 25(OH)D levels. Baseline 6 month 1 year winter summer winter
    • Relationship of 25-hydroxyvitamin D and asthma control in children Lewis, Ann Allergy Asthma Immunol 2012;108:281 Effects of season and 20 patients, 6-17 years with vitamin D supplementation on physician diagnosis of chronic Asthma Control Test scores persistent asthma and current daily controller asthma medication.  Vitamina D supplement  Placebo Placebo or 1,000 IU of vitamin D daily. At initial (winter), 6-month (summer) and 1-year (winter) Visits, BMI, ACT score, spirometry, and serum 25(OH)D levels. Baseline 6 month 1 year winter summer winter
    • Relationship of 25-hydroxyvitamin D and asthma control in children Lewis, Ann Allergy Asthma Immunol 2012;108:281 Effects of season and 20 patients, 6-17 years with vitamin D supplementation on physician diagnosis of chronic FEV1 persistent asthma and current daily controller asthma medication.  Vitamina D supplement  Placebo Placebo or 1,000 IU of vitamin D daily. At initial (winter), 6-month (summer) and 1-year (winter) Visits, BMI, ACT score, spirometry, and serum 25(OH)D levels. Baseline 6 month 1 year winter summer winter
    • Relationship of 25-hydroxyvitamin D and asthma control in children Lewis, Ann Allergy Asthma Immunol 2012;108:281 Effects of season and 20 patients, 6-17 years with vitamin D supplementation on physician diagnosis of chronic FEV1 persistent asthma and Vitamin D current daily controller supplementation asthma medication.   Vitamina D supplement Placebo did not Placebo or affect the ACT 1,000 IU of vitamin D daily. score or FEV1. At initial (winter), 6-month (summer) and 1-year (winter) Visits, BMI, ACT score, spirometry, and serum 25(OH)D levels. Baseline 6 month 1 year winter summer winter
    • Relationship of 25-hydroxyvitamin D and asthma control in children Lewis, Ann Allergy Asthma Immunol 2012;108:2811. Significant seasonal variation in 25(OH)D levels occurred, emphasizing the importance of obtaining multiple 25(OH)D levels throughout a study to allow for increases in 25(OH)D levels due to sun exposure.2. To assess the therapeutic effect in asthma, a significantly higher dose of vitamin D supplementation will be necessary beyond the recommendation of the Institute of Medicine (600 IU) or the American Academy of Pediatrics (400 IU).
    • Vitamin D3 deficiency enhances allergen-inducedlynphocyte responses in a mouse model of allergic airway disease Gorman, Pediatr Allergy Immunol 2012;23:83 24 h after airway challenge with OVA Using 2.26% dietary restriction The ability of vitamin airway-drainingD3-deficient lymphnode cells toBALB/c mice proliferate and secrete Adult offspring born cytokines in response to to vitamin OVA was significantly D3-deficient mothers enhanced
    • • Complementary Medicine
    • Complementary and Alternative Therapies: Use in Pediatric Pulmonary Medicine Chung Pediatr Pulmonol 2011;46:530 Several individual herbs with relevance to pulmonary disease are of particular interest.1. Boswellia serrata have been shown to inhibit pro-inflammatory processes by their effects on 5-lipoxygenase and cyclo-oxygenase and on the complement system.2. Tylophora indica is thought to have antiinflammatory activity.3. Curcumin is probably the most recognized of herbs with potential use in Cystic Fibrosis, largely due to studies showing that it can open cystic fibrosis transmembrane conductance regulator chloride channels. Immunomodulatory effects include down regulation of various proinflammatory cytokines.
    • Herbal medicine treatment reduces inflammation in a murine model of cockroach allergen–induced asthma Kim Ann Allergy Asthma Immunol 2011;107:154 A house dust extract containing endotoxin and cockroach allergens was used for immunization and 2 additional pulmonary challenges Mice were treated with a traditional Korean medicine, So-Cheong-Ryong-Tang (SCRT) or vehicle 1 hour before each pulmonary challenge1) SCRT treatment significantly reduced the hyperreactivity of the airways.2) Inflammation was significantly inhibited by SCRT treatment.
    • Herbal medicine treatment reduces inflammation in a murine model of cockroach allergen–induced asthma Kim Ann Allergy Asthma Immunol 2011;107:154•A Korean herbal medicine, So-Cheong-Ryong-Tang (SCRT, also known asXiao-Qing-Long-Tang in traditional Chinese medicine and as Sho-seiryu-to inJapanese Kampo medicine), has long been prescribed for the treatment ofallergic diseases in Korea, China, and Japan.•During the past decades, studies have demonstrated the potential efficacy ofSCRT in asthma in vivo, in vitro, and in clinical studies.•In vitro, SCRT corrects the TH2-dominant pathologic disorder by suppressingTH2 cell development via reduction of interleukin (IL)-4 expression andpromoting TH1 cell development through increasing interferon-γ expression inmice.•SCRT treatment reduced airway and pulmonary infiltration of eosinophilsinduced by allergen challenge in guinea pigs and mite-sensitized mice, althoughthe mechanisms were not described.•In vitro studies showed that SCRT reduces the release ofhistamine, leukotrienes from mast cells, and tumor necrosis factor α (TNF-α)from peripheral mononuclear cells.
    • Danggui Buxue Tang attenuates eosinophil infiltration and airway hyperresponsiveness in asthmatic mice Ching-Che Lin Ann Allergy Asthma Immunol 2011;107:501 Danggui Buxue Tang (DBT), an herbal formula containing Angelica sinensis (AS) and Astragalus membranaceus (1:5) used in Chinese medicine from days 21 to 27. Sensitized and Suppressed airwaychallenged with OVA hyperresponsiveness and eosinophil infiltration in bronchoalveolar lavage fluid (BALF) and lung, and Th2- associated cytokines and chemokines were inhibited in BALF.
    • Effects of aqueous extract of Echinodorus grandifloruson the immune response in ovalbumin-induced pulmonaryallergy. Brugiolo Ann Allergy Asthma Immunol 2011;106:481 Echinodorus grandiflorus, a plant used in folk medicine for its diuretic and anti- inflammatory properties from day 32 to day 40. BALB/c mice sensitized and nasally challenged with ovalbumin Oral treatment with the extract markedly reduced the number of total cells and eosinophils in bronchoalveolar lavage.
    • Effects of aqueous extract of Echinodorus grandifloruson the immune response in ovalbumin-induced pulmonaryallergy. Brugiolo Ann Allergy Asthma Immunol 2011;106:481 •Echinodorus grandiflorus is an herbaceous plant, popularly known as chapéu-de-couro, that is common in Brazil, Argentina, and Uruguay. •The leaf tea is used by the population mainly as a diuretic, astringent, antirheumatic, depurative, anti-inflammatory, antinociceptive, and arteriosclerosis preventative. •The in vitro and in vivo effects demonstrated for the various extracts of E grandiflorus include anti-inflammatory, analgesic, antihypertensive, diuretic, vasodilator, antimicrobial, and cholesterol reduction.
    • • protective factors for atopic diseases: -life-style
    • Farming in childhood, diet in adulthood and asthma history. Varraso R, Eur Respir J 2012;39:67 In subjects having farmer parents OR for The association of 1.0 – farming lifestyle in childhood and asthma. 0.72 Whether diet in adulthood 0.5 – modifies the association 0.54 between farming lifestyle in childhood and adult-onset asthma. 0.0 54,018 females; childhood adult age 43–68 yrs. onset asthma
    • Farming in childhood, diet in adulthood and asthma history. Varraso R, Eur Respir J 2012;39:67 Association between farmer parents and adult-onsetDietary patterns developed using asthma, according to tertiles of dietary patternsprincipal component analysis: a „„prudent‟‟ pattern (high intake of fruit and vegetables), a „„Western‟‟ pattern (high intake of pizza/salty pies, desserts, cured meats and pasta) and a „„nuts and wine‟‟ pattern (high intake of nuts and seeds, salty biscuits, olives, wine and fortified wine)
    • Farming in childhood, diet in adulthood and asthma history. Varraso R, Eur Respir J 2012;39:67 Association between farmer parents and adult-onset asthma, The associationDietary patterns developed using according to tertiles of dietary patterns betweenprincipal component analysis: a „„prudent‟‟ pattern farmer parents (high intake of fruit and and adult-onset vegetables), a „„Western‟‟ pattern not asthma was modified by diet (high intake of pizza/salty pies, desserts, cured meats in adulthood and pasta) and a „„nuts and wine‟‟ pattern (high intake of nuts and seeds, salty biscuits, olives, wine and fortified wine)
    • Farming in childhood, diet in adulthood and asthma history. Varraso R, Eur Respir J 2012;39:67 Association between Results extend farmer parents and adult-onset previousDietary patterns developed using asthma, according to tertiles of dietary patternsprincipal observations in component analysis: younger cohorts on a „„prudent‟‟ pattern the protective role (high intake of fruit and vegetables), of contact with a „„Western‟‟ pattern livestock and (high intake of pizza/salty farming lifestyle on pies, desserts, cured meats asthma, and pasta) and in particular during a „„nuts and wine‟‟ pattern childhood (high intake of nuts and seeds, salty biscuits, olives, wine and fortified wine)
    • Lifestyle factors and sensitization in children – the ALADDIN birth cohort Stenius, Allergy 2011;66:1330 Background: Several cross-sectional studies indicate that an anthroposophic lifestyle reduces the risk of allergy in children. We initiated the Assessment of Lifestyle and Allergic Disease During Infancy (ALADDIN) birth cohort to elucidate the role of specific factors supposed to mediate this effect. The aims of this study are to describe the ALADDIN cohort and to report patterns of exposure and allergic sensitization during the first years of life.
    • Lifestyle factors and sensitization in children – the ALADDIN birth cohort Stenius, Allergy 2011;66:1330 OR for sensitization in children 330 children from families 1.0 – with anthroposophic, partly anthroposophic, or nonanthroposophic 0.5 – lifestyle. 0.31 Repeated questionnaries. 0. 0.25 p= 0.002 p= 0.004 Follow up 24 months of age. 0 Anthroposophic Partly lifestyle anthroposophic lifestyle
    • Lifestyle factors and sensitization in children – the ALADDIN birth cohort Stenius, Allergy 2011;66:1330 OR for sensitization in children 330Identifying the children from families 1.0 – factors responsible with anthroposophic, for this partly anthroposophic, association or nonanthroposophic 0.5 – (such as lifestyle. diet, medication, a 0.31 Repeatedplace of nd questionnaries. 0.25 p= 0.002 delivery) would be 0. p= 0.004 of significant Follow up 24 months of age. clinical importance 0 Partly Anthroposophic lifestyle anthroposophic lifestyle
    • Non-digestible oligosaccharides reduce immunoglobulinfree light-chain concentrations in infants at risk forallergy. Schouten Pediat Allergy Immunol 2011;22:537 A special prebiotic mixture (Immunofortis®) of short-chain galacto-oligosaccharides (scGOS) and long-chain fructo- oligosaccharides (lcFOS) can reduce the cumulative incidence of atopic dermatitis (AD) in infants at risk for allergy. Immunoglobulin free light-chain (Ig-fLC) might be involved in the pathophysiology of allergic disease. Increased Ig-fLC concentrations were found in patients suffering from AD, cow‟s milk allergy, allergic rhinitis, or asthma.
    • Non-digestible oligosaccharides reduce immunoglobulin free light-chain concentrations in infants at risk for allergy. Schouten Pediat Allergy Immunol 2011;22:537 Kappa Immunoglobulin free light-chain (Ig-fLC) concentrations in atopic dermatitis (AD) (SCORAD+, AD positive) vs. healthy (SCORAD−, AD negative) infants. A plasma kappa and lambda Ig-fLC concentrations. p<0.01 infants at risk for developing allergic disease received a hypoallergenic whey formula containing 8 g/l of the scGOS/lcFOS mixture (n = 34) or maltodextrin as a placebo (n = 40) for 6 months.
    • Non-digestible oligosaccharides reduce immunoglobulinfree light-chain concentrations in infants at risk forallergy. Schouten Pediat Allergy Immunol 2011;22:537 (A) kappa and (B) lambda immunoglobulin free light-chains in infants at high risk for allergy at 6 months of age. A B p<0.001 p<0.001
    • Non-digestible oligosaccharides reduce immunoglobulinfree light-chain concentrations in infants at risk forallergy.ImmunoglobulinPediatlight-chains are produced by Schouten free Allergy Immunol 2011;22:537 (A) kappa and (B) lambda cells, and cause degranulation after B cells, bind to mast immunoglobulin free light-chains in infants second allergenrisk for allergy at 6 months of age. type of at high encounter causing an immediate A allergic response. Redegeld FA, Nat Med 2002;8:694 B p<0.001 p<0.001
    • Temporal variations in early gut microbial colonizationare associated with allergen-specific immunoglobulin E but not atopic eczema at 2 years of age Storrø CEA 2011;41:1545BackgroundIntestinal microbiota undergoes substantial development duringthe first 2 years of life, important for intestinal immunologicdevelopment and maturation influencing systemic immuneresponses.ObjectiveWe aimed to investigate, using a prospective study design,whether allergen-specific IgE and atopic eczema are associatedwith variations in gut microbial colonization patterns in anunselected population during the first 2 years of life.
    • Temporal variations in early gut microbial colonization are associated with allergen-specific immunoglobulin E but not atopic eczema at 2 years of age Storrø CEA 2011;41:1545 Mean microbial concentration in faeces from sensitized (sIgE>0.35 kU/mL) and non-sensitized (sIgE<0.10 kU/mL) children 94 infants sampled from 10 days to 2 years of age. from 10 A days, 4 months, 1 and 2 years postnatal analysed for 12 different bacterial species by quantitative real-time PCR.
    • Temporal variations in early gut microbial colonization are associated with allergen-specific immunoglobulin E but not atopic eczema at 2 years of age Storrø CEA 2011;41:1545 Mean microbial concentration in faeces from sensitized (sIgE>0.35 kU/mL) and Subjects with 94 infants sampled non-sensitized (sIgE<0.10 kU/mL) children from 10 days to 2 years of age. fromatopic 10 days, A 4sensitization months, 1 and 2 years postnatal had lower levels analysed for 12 of Escherichia different bacterial coli species by at 4 months quantitative real-timeyear. and 1 PCR.
    • Temporal variations in early gut microbial colonization are associated with allergen-specific immunoglobulin E but not atopic eczema at 2 years of age Storrø CEA 2011;41:1545 Mean microbial concentration in faeces from sensitized (sIgE>0.35 kU/mL) and non-sensitized (sIgE<0.10 kU/mL) children 94 infants sampled from 10 days to 2 years of age. from 10 days, B 4 months, 1 and 2 years postnatal and analysed for 12 different bacterial species by quantitative real-time PCR.
    • Temporal variations in early gut microbial colonization are associated with allergen-specific immunoglobulin E but not atopic eczema at 2 years of age Storrø CEA 2011;41:1545 Mean microbial concentration in faeces from sensitized (sIgE>0.35 kU/mL) and non-sensitized (sIgE<0.10 kU/mL) children 94 infants sampled from 10 days to 2 years of age. from 10 days, C 4 months, 1 and 2 years postnatal and analysed for 12 different bacterial species by quantitative real-time PCR. Age
    • Temporal variations in early gut microbial colonization are associated with allergen-specific immunoglobulin E but not atopic eczema at 2 years of age Storrø CEA 2011;41:1545 Mean microbial concentration in faeces from sensitized (sIgE>0.35 kU/mL) and non-sensitized (sIgE<0.10 kU/mL) children 94 infants sampled from 10 days to 2 years of age. from 10 days, C We found no 4 months, 1 and association between 2 years postnatal colonization pattern and analysed for and atopic eczema. 12 different bacterial species by quantitative real-time PCR. Age
    • Regulation of Inflammatory Responses by the Commensal Microbiota. Marsland, Thorax 2012;67:931. Fermentation of dietary fibre by intestinal bacteria has long been known to yield short-chain fatty acids (SCFAs) such as acetate, propionate and butyrate.2. These are largely produced within the colon and, when applied as enemas, they have shown efficacy as a treatment for inflammatory bowel disease.3. Intestinal microbiota can influence inflammation at peripheral sites including the lung.
    • Regulation of Inflammatory Responses by the Commensal Microbiota. Marsland, Thorax 2012;67:93 Control of pulmonary inflammation Short-chain fatty acids by commensal bacteria. (SCFAs) are potent suppressors of inflammation via their signalling through GPR43 receptor on immune cells such as granulocytes. SCFA can act locally in the intestine to dampen inflammation but can also regulate inflammationin peripheral tissues such as the lung. Recent findings suggest that the lung harbours a microbiota which may also act to regulate pulmonary inflammation, although the mechanisms by which this regulation occurs remain to be fully unravelled.
    • Regulation of Inflammatory Responses by the Commensal Microbiota. Marsland, Thorax 2012;67:93A. It has classically been believed that healthy airways are sterile.B. Evidence emerging from the use of molecular techniques now indicates that the airways themselves do harbour a bacterial microbiota and that the make-up of this microbial community changes depending upon the health status of the individual.C. A „healthy‟ lung, for example, has been associated with bacteria of the Bacteroidetes phylum while Proteobacteria were over-represented in the lungs of individuals with asthma or chronic obstructive pulmonary disease.
    • Regulation of Inflammatory Responses by the Commensal Microbiota. Marsland, Thorax 2012;67:93A. It has classically been believed that healthy airways are sterile.B. Evidence emerging from the use of molecular techniques It is likely that either direct exposure now indicates that the airways themselves do harbour to bacteria or colonisation with a bacterial microbiota and that the make-up of this distinct bacterialdepending upon could microbial community changes communities protect of lung from the health statusthethe individual.inflammation or, on the other hand, perpetuate disease.C. A „healthy‟ lung, for example, has been associated with bacteria of the Bacteroidetes phylum while Proteobacteria were over-represented in the lungs of individuals with asthma or chronic obstructive pulmonary disease.
    • Lung function decline in relation to mould and dampness in the home: the longitudinal European Community Respiratory Health Survey ECRHS II Norbäck Thorax 2011;66:396 % of houses with Participants in the 50 – European Respiratory 50.1% Health Survey initially examined aged 20-45 yrs 40 – 41.3% and 9 yrs later (n=6443). 30 – Dampness (water damage 20 – or damp spots) and indoor mould, ever and in 10 – the last 12 months. 0 Any dampness Indoor mould
    • Lung function decline in relation to mould and dampness in the home: the longitudinal European Community Respiratory Health Survey ECRHS II Norbäck Thorax 2011;66:396 Additional decline in FEV1 ml/year 0 Participants in the European Respiratory -2.25 Health Survey initially examined aged 20-45 yrs and 9 yrs later (n=6443). -5 Dampness (water damage -7.43 or damp spots) and indoor mould, ever and in the last 12 months. -10 Women with In women with dampness observed damp spots at home in the bedroom
    • Lung function decline in relation to mould and dampness in the home: the longitudinal European Community Respiratory Health Survey ECRHS II Norbäck Thorax 2011;66:396 Additional decline in FEV1 ml/year 0 Participants in the Dampness and Europeanmould growth indoor Respiratory -2.25 Health Survey initially is common in examined aged 20-45 yrs dwellings, and the andpresence of(n=6443). 9 yrs later damp -5 is a risk factor for Dampness (water damage lung function decline, -7.43 orespecially in women. damp spots) and indoor mould, ever and in the last 12 months. -10 Women with In women with dampness observed damp spots at home in the bedroom
    • Lung function decline in relation to mould and dampness in the home: the longitudinal European Community Respiratory Health Survey ECRHS II Norbäck Thorax 2011;66:3961) The additional mean lung function decline, -2.25 ml/year for self-reported dampness and -7.43 ml/year for observed dampness in the bedroom, is of the same order of magnitude as estimated for moderate tobacco smoking in the same ECRHS cohort.2) The reason for the sex difference in effect remains unclear, but could be due to either higher susceptibility or a longer exposure time in the dwelling for women.
    • Lung function prior to viral lower respiratory tract infections in prematurely born infants Drysdale Thorax 2011;66:468ObjectivePrematurely born infants who develop respiratory syncytial virus(RSV) lower respiratory tract infections (LRTIs) have lungfunction abnormalities at follow-up.The aim of this study was to determine whether prematurely borninfants who developed symptomatic RSV, or other viral LRTI(s),had poorer premorbid lung function than infants who did notdevelop LRTIs during the RSV season. ?
    • Lung function prior to viral lower respiratory tract infections in prematurely born infants Drysdale Thorax 2011;66:468 Functional residual capacity (FRC), compliance (Crs) and resistance (Rrs) of the respiratory system measured % infants developing LRTs at 36 weeks postmenstrual age. 50 – Nasopharyngeal aspirates whenever the infants had an LRTI. RSV A and RSV B, rhinovirus, 40 – 46% influenza A and B, 30 – 73/159 parainfluenza 1, 2 and 3, human metapneumovirus and 20 – adenovirus. 159 infants with a median gestational 10 – age of 34 (range 23-36) weeks prospectively followed. 0
    • Lung function prior to viral lower respiratory tract infections in prematurely born infants Drysdale Thorax 2011;66:468 Functional residual capacity (FRC), compliance (Crs) and resistance (Rrs) of the respiratory system measured Overall, there were at 36 weeks postmenstrual age. no significant differences Nasopharyngeal aspirates whenever in the FRC (p=0.54), the infants had an LRTI. Crs (p=0.11) or RSV A and RSV B, rhinovirus, Rrs (p=0.12) results influenza A and B, between those who parainfluenza 1, 2 and 3, developed an RSV human metapneumovirus and or other viral LRTI adenovirus. and those who did not 159 infants with a median gestational develop an LRTI. age of 34 (range 23-36) weeks prospectively followed. …but…
    • Lung function prior to viral lower respiratory tract infections in prematurely born infants Drysdale Thorax 2011;66:468 Functional residual capacity (FRC), compliance (Crs) and resistance (Rrs) of the respiratory system measured at 36 weeks postmenstrual Infants with RSV age. or other viral LRTIs Nasopharyngeal aspirates whenever who were admitted to the infants had an LRTI. hospital compared with those who RSV A and RSV B, rhinovirus, influenza A and were not had higher B, parainfluenza 1, 2 and Rrs results (p=0.033 and 3, human p=0.039, respectively). metapneumovirus and adenovirus. 159 infants with a median gestational age of 34 (range 23-36) weeks prospectively followed.
    • Lung function prior to viral lower respiratory tract infections in prematurely born infants Drysdale Thorax 2011;66:468 Functional residual capacity (FRC), compliance (Crs) and resistance (Rrs) Diminished of the respiratory system measured at 36premorbid lung weeks postmenstrual age. Infants with RSV or other viral LRTIs function Nasopharyngeal aspirates whenever who were admitted to the infants had an LRTI. may predispose hospital compared RSV A and RSV B, rhinovirus, prematurely born influenza A and B, with those who parainfluenza 1, to severe were not had higher infants 2 and 3, and human metapneumovirus Rrs results (p=0.033 and adenovirus. LRTIs in viral p=0.039, respectively). infancy. 159 infants with a median gestational age of 34 (range 23-36) weeks prospectively followed.
    • Factors influencing asthma remission: a longitudinal study from childhood to middle age Burgess Thorax 2011;66:508 % patients with asthma remission 80 – In 1968 the Tasmanian Longitudinal Health Study 70 – enrolled 7-year-old 65% 60 – schoolchildren (n=8583). 50 – Re-surveyed in 2004. 40 – Asthma remission, defined as 30 – no asthma attack for 2 years 20 – and no current asthma medication. 10 – 0
    • Factors influencing asthma remission: a longitudinal study from childhood to middle age Burgess Thorax 2011;66:508 OR for remission1.0 – 0.750.5 – 0.66 0.66 0.66 0.56 0.42 0.380.0 childhood passive childhood later-onset childhood later-onset maternal allergic rhinitis allergic rhinitis eczema eczema asthma chronic bronchitis smoking
    • Factors influencing asthma remission: a longitudinal study from childhood to middle age Burgess Thorax 2011;66:508 OR for remission. Childhood-onset asthma (OR=3.76)1.0 – was more likely to remit than adult-onset asthma 0.750.5 – 0.66 0.66 0.66 0.56 0.42 0.380.0 childhood passive childhood later-onset childhood later-onset maternal allergic rhinitis allergic rhinitis eczema eczema asthma chronic bronchitis smoking
    • Factors influencing asthma remission: a longitudinal study from childhood to middle age Burgess Thorax 2011;66:508ConclusionWhile inherited factors cannot be changed,the effect of allergic rhinitis or eczemaon asthma remission might be altered by early,aggressive treatment.Every effort should be made to lessenpassive exposure to tobacco smoke.
    • Nocturnal asthma monitoring by chest wall electromyography Steier Thorax 2011;66:609RationalePatients with suboptimal asthma control often havenocturnal symptoms which wake them, causingsleep fragmentation.ObjectivesIt was hypothesised that symptomatic patients were moreaccurately identified by measuring respiratory effort usingchest wall electromyography than by pulmonary functiontesting.
    • Nocturnal asthma monitoring by chest wall electromyography Steier Thorax 2011;66:609 Nocturnal electricalactivity of the parasternal An elevated respiratoryintercostal muscles disturbance index (RDI)(EMGpara); was associated with poor Subjects with controlled asthma control(diurnal peak expiratory flow (RDI in normals 0.5,(PEF) variability <20%, n=12) in controlled asthma 4.0and uncontrolled (diurnal p<0.001,PEF variability >20%, n=12) and in poorly controlledasthma; asthma 7.4 p<0.021). Normal subjects (n=12).
    • Nocturnal asthma monitoring by chest wall electromyography Steier Thorax 2011;66:609 Nocturnal electricalactivity of the parasternal An elevated respiratoryintercostal muscles disturbance index (RDI)(EMGpara); was associated with poor Subjects with controlled asthma control(diurnal peak expiratory flow (RDI in normals 0.5,(PEF) variability <20%, n=12) in controlled asthma 4.0and uncontrolled (diurnal p<0.001,PEF variability >20%, n=12) and in poorly controlledasthma; asthma 7.4 p<0.021). Normal subjects (n=12).
    • Nocturnal asthma monitoring by chest wall electromyography Steier Thorax 2011;66:609 Polysomnography dataRDI, respiratory disturbance index, non-normally distributed and presented as median (IQR);REM, rapid eye movement; TST, total sleep time.*Difference between normal group versus uncontrolled asthma (p=0.005) and controlled vs uncontrolled asthma(p=0.038). Ɨ Significant difference (p<0.001).
    • Nocturnal asthma monitoring by chest wall electromyography Steier Thorax 2011;66:609 Polysomnography dataRDI, respiratory disturbancewas no significant difference presented assleep time, but 1) there index, non-normally distributed and in overall median (IQR);REM, rapid eye movement; TST, total sleep time. reduced in uncontrolled asthma and 2) REM sleep duration was*Difference between normal group versus uncontrolled asthma (p=0.005) and controlled vs uncontrolled asthma 3) RDI was elevated in those with asthma.(p=0.038). Ɨ Significant difference (p<0.001).
    • Bacterial-induced protection against allergic inflammation through a multicomponent immunoregulatory mechanism Nembrini Thorax 2011;66:755 1) Exposed mice to the bacterium Escherichia coli 2) Sensitization and intranasal challenge with ovalbumin Pulmonary exposure to the bacterium Escherichia coli leads to a suppression of (-) allergic airway inflammation. allergic airway inflammation
    • Bacterial-induced protection against allergic inflammation through a multicomponent immunoregulatory mechanism Nembrini Thorax 2011;66:755 1) Exposed mice to the bacterium Escherichia coli 2) Sensitization and intranasal challenge with ovalbumin modulation was neither This immune mediated by the induction of a T helper 1 (Th1) response nor regulatory T cells; however, it was Pulmonary exposure to the bacterium dependent on Toll-like receptor 4 Escherichia coli leads to a suppression of (-) (TLR4) airwaydid not involve TLR allergic but inflammation. desensitisation. allergic airway inflammation
    • Bacterial-induced protection against allergic inflammation through a multicomponent immunoregulatory mechanism Nembrini Thorax 2011;66:755 Dendritic cells in 1) Exposed mice to the bacterium the lung displayed Escherichia coli a less activated 2) Sensitization and intranasal challenge phenotype and had impaired antigen with ovalbumin modulation was neither This immune presentation mediated by the induction of a capacity. T helper 1 (Th1) response nor Consequently, in regulatory T cells; however, it was Pulmonary exposure to the bacterium situ Th2 cytokine dependent on Toll-like receptor 4 Escherichia coli leads to a suppression of production was (-) (TLR4) airwaydid not involve TLR allergic but inflammation. abrogated desensitisation. allergic airway inflammation
    • Asthma protection with bacteria – science or fiction? Renz Thorax 2011;66:744 Infants living in a microbial-rich environment show a high degree of protection, particularly against respiratory allergies and allergic sensitisation; That microbes are indeed relevant in triggering the protective immune response was epidemiologically shown initially for exposure to lipopolysaccharide (LPS), a membrane component of Gram-negative bacteria;
    • Asthma protection with bacteria – science or fiction? Renz Thorax 2011;66:744 Not only Gram-negative but also Gram-positive bacteria were able to provide this protection; This effect is not even restricted to bacterial compounds, since recently it was observed that even the plant product arabinogalactan can induce this protective effect8. 8. Peters M, Kauth M, Scherner O, et al. Arabinogalactan isolated from cowshed dust extract protects mice from allergic airway inflammation and sensitization. J Allergy Clin Immunol 2010;126:648e56, e1e4.
    • Asthma protection with bacteria – science or fiction? Renz Thorax 2011;66:744 Concerning the mucosal aspects, the immune response is initiated by the recognition of microbial compounds by pattern recognition receptors (PRRs); The Toll-like receptor (TLR) family represents one important group of such PRRs
    • Epigenetic regulation in murine offspring as a novelmechanism for transmaternal asthma protection induced by microbes Brand JACI 2011;128:618 Exposed to the farm-derived gram-negative bacterium Acinetobacter lwoffii F78. Pregnant maternal mice Epigenetic modifications in the offspring were analyzed in TH1- and TH2-relevant genes of CD4+ T cells.
    • Epigenetic regulation in murine offspring as a novelmechanism for transmaternal asthma protection induced by microbes Brand JACI 2011;128:618 Exposed to the farm-derived gram-negative bacterium Acinetobacter lwoffii F78. Prenatal administration of A lwoffii A78 Pregnant maternal mice prevented the development of an asthmatic phenotype in the progeny, and this effect was Epigenetic modifications in the IFN-γ dependent. offspring were analyzed in TH1- and TH2-relevant genes of CD4+ T cells.
    • Epigenetic regulation in murine offspring as a novelmechanism for transmaternal asthma protection induced by microbes Brand JACI 2011;128:618 Exposed to the farm-derived gram-negative bacterium Acinetobacter lwoffii F78. The IFNG promoter of CD4+ T cells in the offspring Pregnant maternal mice revealed a significant protection against loss of histone 4 (H4) acetylation, which was closely Epigenetic modifications in the associated with offspring were analyzed in TH1- and IFN-γ expression. TH2-relevant genes of CD4+ T cells.
    • Epigenetic regulation in murine offspring as a novel mechanism for transmaternal asthma protection induced by microbes Brand JACI 2011;128:618 Concentration of IFN-γ, IL-4 and IL-5 in the supernatantof anti-CD-3/anti-CD-28-stimulated mononuclear spleen cells from offspring from A lwoffii F78- or sham-exposed (PBS) mothers. p <0.05 p <0.05 p <0.01
    • Epigenetic regulation in murine offspring as a novelmechanism for transmaternal asthma protection induced by microbes Brand JACI 2011;128:618 Relative mRNA expression of IFN-γ, IL-4 and IL-5. p <0.01 p <0.05 p <0.05
    • Epigenetic regulation in murine offspring as a novelmechanism for transmaternal asthma protection induced by microbes Brand JACI 2011;128:618 These data support the hygene concept Relative mRNA expression of IFN-γ, IL-4 and IL-5. and indicate that microbes operate by means of epigenetic mechanisms. p <0.01 p <0.05 p <0.05
    • Reduced diversity of the intestinal microbiota during infancy is associated with increased risk of allergic disease at school age Bisgaard JACI 2011;128:646 Bacterial diversity in the early intestinal flora 1 and 12 months after birth was inversely associated with the Intestinal microbiota risk of allergic sensitization in infants in the Copenhagen (serum specific IgE p =0.003; Prospective Study on skin prick test p =0.017), Asthma and Childhood. peripheral blood eosinophils (p =0.034), and 411 high-risk children allergic rhinitis (p =0.007). followed for 6 yrs. There was no association with Bacterial flora at 1 and 12 the development of asthma months by 16S rRNA PCR. or atopic dermatitis.
    • Intestinal microbial diversity in infancy and allergy risk at school age. Editorial Ege JACI 2011;128:653•Novel techniques that offer the comprehensiveassessment of microbial exposure on a molecular level.•The main principle consists in the amplification of specificmicrobial DNA fragments.•Hence the targeted DNA fragment needs to be distinct fromhuman DNA.•For bacteria, a DNA fragment encoding the 16S subunit of the ribosomal RNA (16S rRNA) can be used becauseit is unique to bacterial and varies even between genera andspecies.
    • Effects of Helicobacter pylori, geohelminth infection and selected commensal bacteria on the risk of allergicdisease and sensitization in 3-year-old Ethiopian children Amberbir CEA 2011;41:1422 % children infected with 50 878 children in a – population-based birth. 41% 40 Followed up at age 3. – SPTs. 30 – 8.5% H. Pylory Geohelminths 20
    • Effects of Helicobacter pylori, geohelminth infection and selected commensal bacteria on the risk of allergicdisease and sensitization in 3-year-old Ethiopian children Amberbir CEA 2011;41:1422 % children infected with 50 H. pylori infection was 878 children in a reduced associated with population- – based birth. eczema risk of 41% 40 (OR 0.49, P=0.05) Followed up at age 3. and D. pteronyssinus – sensitization Allergen skin. P=0.07) (OR 0.42, 30 – 8.5% H. Pylory Geohelminths 20
    • Migration and asthma medication in international adoptees and immigrant families in Sweden Bråbäck CEA 2011;41:1108 The risk of purchased prescribed inhaled 24 252 international corticosteroids by age at adoption. adoptees. A 47 986 foreign-born and 40 971 Swedish-born with foreign-born parents. 1 770 092 Swedish-born residents with Swedish-born parents (age 6–25 years). Purchased prescribed ICS during 2006 used as an indicator of asthma. Red circles: Or after adjustment for sex, geographical residency (urban/rural) and region of birth. Blue squares = unadjusted OR
    • Migration and asthma medication in international adoptees and immigrant families in Sweden Bråbäck CEA 2011;41:1108 The risk of purchased prescribed inhaled 24 252 international corticosteroids by age at immigration. adoptees. B 47 986 foreign-born and 40 971 Swedish-born with foreign-born parents. 1 770 092 Swedish-born residents with Swedish-born parents (age 6–25 years). Purchased prescribed inhaled corticosteroids (ICS) during 2006 were used as an Red circles: Or after adjustment for sex, geographical residency (urban/rural) and indicator of asthma. region of birth. Blue squares = unadjusted OR
    • Migration and asthma medication in international adoptees and immigrant families in Sweden Bråbäck CEA 2011;41:1108 The risk of purchased prescribed inhaled 24 252 international corticosteroids by age at immigration. Age at immigration is adoptees. B a more important 47 986 foreign-born and determinant of purchased 40 ICS Swedish-born with 971 than population of foreign-born parents. origin. This indicates 1 770 the importance of 092 Swedish-born residents with Swedish-born environmental factors for parents (age 6–25 years). asthma in schoolchildren Purchased young adults. and prescribed inhaled corticosteroids (ICS) during 2006 were used as an Red circles: Or after adjustment for sex, geographical residency (urban/rural) and indicator of asthma. region of birth. Blue squares = unadjusted OR
    • Identification of a Dau c PRPlike protein (Dau c 1.03)as a new allergenic isoform in carrots (cultivar Rodelika). Wangorsch, Clin Exp Allergy 2012;42:156 1) Carrot (Daucus carota) allergy is one of the most common types of birch pollen-related food allergy in central Europe. 2) Approximately 24% of food allergic subjects suffer from allergic symptoms after ingestion of carrots. 3) Adverse reactions to carrots are elicited due to cross-reactive IgE-epitopes between the major birch pollen allergen, Bet v 1 and homologous food proteins. 4) Bet v 1 and the major carrot allergen Dau c 1 belong to the family of pathogenesis related proteins 10 (PR-10).
    • Identification of a Dau c PRPlike protein (Dau c 1.03)as a new allergenic isoform in carrots (cultivar Rodelika). Wangorsch, Clin Exp Allergy 2012;42:156 •The Dau c PRPlike proteinObjective To investigate was identified as a newpotential allergenic properties allergenic isoform, Dau cof a Dau c PRPlike protein, 1.03, in carrot roots.a novel isoform of thepathogenesis related proteins •68% of carrot allergic10 (PR-10) protein family in patients were sensitized tocarrot. rDau c 1.03.
    • Identification of a Dau c PRPlike protein (Dau c 1.03)as a new allergenic isoform in carrots (cultivar Rodelika). Wangorsch, Clin Exp Allergy 2012;42:156 Dau c 1.03 appears •The Dau c PRPlike protein to contribute to the was identified as a newObjective To investigate allergenicity allergenic isoform, Dau cpotential carrots and should of allergenic properties 1.03, in carrot roots.of a Dau cbe considered PRPlike protein,a novel isoform ofsilencing for gene the PR-10 •68% of carrot allergicprotein family in carrot. of carrot allergens. patients were sensitized to rDau c 1.03.
    • Allergenic activity of different tomato cultivars in tomato allergic subjects. Dölle CEA 2011;41:1643BackgroundTomatoes (Solanum lycopersicum) are consumed worldwide andtheir amount of consumption is associated with the prevalenceof tomato allergy. Therefore, identification of tomato cultivarswith reduced allergenicity would potentially increase the qualityof life of affected subjects.ObjectiveIn this study, we examined the allergenic and biological activityof two different tomato cultivars in tomato allergic subjects.
    • Allergenic activity of different tomato cultivars in tomato allergic subjects. Dölle CEA 2011;41:1643 SPT reactions to ‗Reisetomate‘ (RT) and ‗Matina‘ (MT). The median is depicted as 25 subjects with black line, and outliers are shown as dots. tomato allergy. A Skin prick test and DBPCFC to investigate the clinical differences between two tomato cultivars („Reisetomate‟ and „Matina‟).
    • Allergenic activity of different tomato cultivars in tomato allergic subjects. Dölle CEA 2011;41:1643 Symptom severity expressed as sum scores, no clinical relevant allergy ×0, mild 25 subjects with allergy ×1, moderate allergy ×2 and severe allergy tomato allergy. ×3. B Skin prick test and DBPCFC to investigate the clinical differences between two tomato cultivars („Reisetomate‟ and „Matina‟).
    • Allergenic activity of different tomato cultivars in tomato allergic subjects. Dölle CEA 2011;41:1643 Symptom severity expressed as sum scores, no clinical relevant allergy ×0, mild allergy ×1, 25 subjects cultivars Tomato with moderate allergy ×2 and severe allergy ×3. promote a distinct tomato allergy. clinical reactivity in B Skin tomato allergic prick test and DBPCFC to might be subjects. This investigate the due to instabilities of clinical differences physicochemical sensitive two tomato between proteins and/or cultivars different isoform („Reisetomate‟ expression of allergens. and „Matina‟).
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