Helicobacter pylori infection causes gastritis and peptic ulcers and is associated with increased levels of proinflammatory cytokines tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ). The study evaluated 148 patients with gastritis or peptic ulcers, finding high rates of positive IgG antibodies to H. pylori and its virulence factor CagA. Levels of TNF-α and IFN-γ were significantly higher in infected patients compared to controls, indicating their role in gastric inflammation caused by H. pylori. Estimating IgG levels and CagA positivity provides good immunodiagnostic markers for these diseases before endoscopy.
Laboratory diagnosis of H. Pylori infection, Ola ElgaddarOla Elgaddar
A short presentation for the different laboratory techniques used in diagnosing Helicobacter Pylori infection. A special focus is given for the diagnostic performance of every test.
Laboratory diagnosis of H. Pylori infection, Ola ElgaddarOla Elgaddar
A short presentation for the different laboratory techniques used in diagnosing Helicobacter Pylori infection. A special focus is given for the diagnostic performance of every test.
Enterocin 55 produced by non rabbit-derived strain Enterococcus faecium EF55 ...Agriculture Journal IJOEAR
— Ent55 is produced by poultry strain Enterococcus faecium EF55. It is substance which can be allotted to Class II enterocins; thermo-stable, small peptide. Because producer strain has shown beneficial effect in poultry and broiler rabbits as well, we decided to apply Ent55 in broiler rabbit husbandry. Ent55 showed antimicrobial activity in broiler rabbits by reduction of staphylococci, Clostridiae, pseudomonads and coliforms. Its beneficial effect was demonstrated by stimulation of phagocytic activity as well as by reduction of Eimeria spp. oocysts. GPx values were lower; it means, no oxidative stress was evoked. Moreover, it has not negative influence on growth performance and biochemical parameters. Our results indicated that enterocin produced by not-autochtonous strain can also have protective and beneficial effect in broiler rabbits.
Immunomodulatory effect of schisandrae oil in mouse model of autoimmune hepat...LucyPi1
Abstract Objective: To study the immunomodulatory effect of schisandra oil (SCO) in mouse model of autoimmune hepatitis induced by concanavalin A (ConA). Methods: C57BL/6 mice were divided into control group, model group and SCO group. Mice in SCO group were given SCO at 5 mg/kg by intragastric administration every day for 7 days, followed by intravenous injection of ConA at 10 mg/kg. 10 hours after ConA injection, the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) were measured by the kits, the expression of inflammatory cytokines like interferon-γ (IFN-γ), interleukin-4 (IL-4), interleukin-17 (IL-17), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) in liver was detected by real-time quantitative PCR, and the T cell activation and IFN-γ expression in spleen and MLN were examined by flow cytometry. Results: Compared with control group, each indicator in model group were significantly higher. In SCO preventive treatment group, the levels of serum ALT, AST and LDH were significantly reduced (all P < 0.001), the expression levels of inflammatory cytokines in liver were downregulated, the T cell activation in spleen and MLN was inhibited (P = 0.006 and P = 0.008), the percentages of IFN-γ+ CD8+ and IFN-γ+ CD4+ T cells were decreased, and the frequencies of Th2 and Th17 cells in spleen and MLN were also decreased at the same time. Conclusion: SCO has a protective effect on immune liver injury by inhibiting the activation of T cells and reducing the expression of inflammatory cytokines, which reflects that SCO plays a role in the immunomodulation of autoimmune hepatitis, indicating that SCO is of great significance for the maintenance of autoimmune homeostasis.
ABSTRACT- This study was an attempt to estimate the prevalence of Antimicrobial resistance in patients attending the OPD and IPD of IIMS&R, hospital, Lucknow. Total 453 urine samples were included in this study. Urinary isolates from symptomatic UTI cases were identified by conventional methods. Of the 453 processed samples 166 samples showed significant colony count of pathogens among which the most prevalent were E. coli (49.39%) followed by Klebsiella species (7.83%). The majority of the isolates were from female (68.67%) while the remaining was from male (31.32%). Dysuria was the most common clinical presentation followed by fever and abdominal pain. Diabetes and urogenital instrumentation were the major risk factors for UTI. Among the 166 urine samples which showed significant colony count, 152 (91.56%) of specimen showed pus cells in wet film examination. Among the gram-negative enteric bacilli high prevalence of resistance was observed against Ampicillin, Cefotaxime, Ciprofloxacin, Nalidixic acid and co-trimoxazole. 44% of isolates were detected to produce ESBL among the gram negative bacteria. Carbapenemase production was seen in 13 (11.71%) isolates. Among the 32 Enterococcus isolates 14 (43.75%) were resistant to High level Gentamicin, 2 (6.25%) were resistant to High level Streptomycin while 12 (37.50%) of isolates were resistant to both of the antimicrobial drugs. Among the 16 Staphylococcus species, 8 (50%) were MRSA.
KEYWORDS- MRSA, Antimicrobial resistance, UTI, ESBL, Gram-negative bacteria
Sensitivity and specificity of 99mTc-UBI29-41 and 67Ga-Citrate scintigraphy i...iosrphr_editor
The IOSR Journal of Pharmacy (IOSRPHR) is an open access online & offline peer reviewed international journal, which publishes innovative research papers, reviews, mini-reviews, short communications and notes dealing with Pharmaceutical Sciences( Pharmaceutical Technology, Pharmaceutics, Biopharmaceutics, Pharmacokinetics, Pharmaceutical/Medicinal Chemistry, Computational Chemistry and Molecular Drug Design, Pharmacognosy & Phytochemistry, Pharmacology, Pharmaceutical Analysis, Pharmacy Practice, Clinical and Hospital Pharmacy, Cell Biology, Genomics and Proteomics, Pharmacogenomics, Bioinformatics and Biotechnology of Pharmaceutical Interest........more details on Aim & Scope).
Asymptomatic urinary tract infection amongst some Students of Michael Okpara ...Premier Publishers
This work was carried out to determine Asymptomatic Urinary Tract Infection amongst some students of Michael Okpara University of Agriculture, Umudike and the sensitivity pattern of the isolates from urine. Using aseptic technique, midstream urine were collected from sixty (60) students, urinalysis was carried out on the urine samples and was then cultured on CLED and MacConkey agar using pour plate method. Growth was observed in 26 (87%) of the sample while there was no growth in 4 (13%) of the sample. Out of the 26 (87%) samples with growth, 14 (47%) had significant bacteria growth while 12 (40%) had no significant growth. Incidence of asymptomatic bacteriuria was higher in females 8 (57%) than males 6 (38%). The organisms isolated were Escherichia coli, Klebsiella species, Staphylococcus saprophyticus, Staphylococcus aureus, Enterococcus faecalis, Proteus species, and Pseudomonas aeruginosa. All the Gram positive isolates were sensitive to Gentamycin and all resistance to Cefuroxime, Ceftazidime, Ceftriaxone, Cloxacillin. The Gram negative isolates were mostly sensitive to Nitrofurantoin, Gentamycin and Ofloxacin. Therefore, these drugs could be considered as the first line of drug for the treatment of asymptomatic urinary tract infection.
Enterocin 55 produced by non rabbit-derived strain Enterococcus faecium EF55 ...Agriculture Journal IJOEAR
— Ent55 is produced by poultry strain Enterococcus faecium EF55. It is substance which can be allotted to Class II enterocins; thermo-stable, small peptide. Because producer strain has shown beneficial effect in poultry and broiler rabbits as well, we decided to apply Ent55 in broiler rabbit husbandry. Ent55 showed antimicrobial activity in broiler rabbits by reduction of staphylococci, Clostridiae, pseudomonads and coliforms. Its beneficial effect was demonstrated by stimulation of phagocytic activity as well as by reduction of Eimeria spp. oocysts. GPx values were lower; it means, no oxidative stress was evoked. Moreover, it has not negative influence on growth performance and biochemical parameters. Our results indicated that enterocin produced by not-autochtonous strain can also have protective and beneficial effect in broiler rabbits.
Immunomodulatory effect of schisandrae oil in mouse model of autoimmune hepat...LucyPi1
Abstract Objective: To study the immunomodulatory effect of schisandra oil (SCO) in mouse model of autoimmune hepatitis induced by concanavalin A (ConA). Methods: C57BL/6 mice were divided into control group, model group and SCO group. Mice in SCO group were given SCO at 5 mg/kg by intragastric administration every day for 7 days, followed by intravenous injection of ConA at 10 mg/kg. 10 hours after ConA injection, the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) were measured by the kits, the expression of inflammatory cytokines like interferon-γ (IFN-γ), interleukin-4 (IL-4), interleukin-17 (IL-17), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) in liver was detected by real-time quantitative PCR, and the T cell activation and IFN-γ expression in spleen and MLN were examined by flow cytometry. Results: Compared with control group, each indicator in model group were significantly higher. In SCO preventive treatment group, the levels of serum ALT, AST and LDH were significantly reduced (all P < 0.001), the expression levels of inflammatory cytokines in liver were downregulated, the T cell activation in spleen and MLN was inhibited (P = 0.006 and P = 0.008), the percentages of IFN-γ+ CD8+ and IFN-γ+ CD4+ T cells were decreased, and the frequencies of Th2 and Th17 cells in spleen and MLN were also decreased at the same time. Conclusion: SCO has a protective effect on immune liver injury by inhibiting the activation of T cells and reducing the expression of inflammatory cytokines, which reflects that SCO plays a role in the immunomodulation of autoimmune hepatitis, indicating that SCO is of great significance for the maintenance of autoimmune homeostasis.
ABSTRACT- This study was an attempt to estimate the prevalence of Antimicrobial resistance in patients attending the OPD and IPD of IIMS&R, hospital, Lucknow. Total 453 urine samples were included in this study. Urinary isolates from symptomatic UTI cases were identified by conventional methods. Of the 453 processed samples 166 samples showed significant colony count of pathogens among which the most prevalent were E. coli (49.39%) followed by Klebsiella species (7.83%). The majority of the isolates were from female (68.67%) while the remaining was from male (31.32%). Dysuria was the most common clinical presentation followed by fever and abdominal pain. Diabetes and urogenital instrumentation were the major risk factors for UTI. Among the 166 urine samples which showed significant colony count, 152 (91.56%) of specimen showed pus cells in wet film examination. Among the gram-negative enteric bacilli high prevalence of resistance was observed against Ampicillin, Cefotaxime, Ciprofloxacin, Nalidixic acid and co-trimoxazole. 44% of isolates were detected to produce ESBL among the gram negative bacteria. Carbapenemase production was seen in 13 (11.71%) isolates. Among the 32 Enterococcus isolates 14 (43.75%) were resistant to High level Gentamicin, 2 (6.25%) were resistant to High level Streptomycin while 12 (37.50%) of isolates were resistant to both of the antimicrobial drugs. Among the 16 Staphylococcus species, 8 (50%) were MRSA.
KEYWORDS- MRSA, Antimicrobial resistance, UTI, ESBL, Gram-negative bacteria
Sensitivity and specificity of 99mTc-UBI29-41 and 67Ga-Citrate scintigraphy i...iosrphr_editor
The IOSR Journal of Pharmacy (IOSRPHR) is an open access online & offline peer reviewed international journal, which publishes innovative research papers, reviews, mini-reviews, short communications and notes dealing with Pharmaceutical Sciences( Pharmaceutical Technology, Pharmaceutics, Biopharmaceutics, Pharmacokinetics, Pharmaceutical/Medicinal Chemistry, Computational Chemistry and Molecular Drug Design, Pharmacognosy & Phytochemistry, Pharmacology, Pharmaceutical Analysis, Pharmacy Practice, Clinical and Hospital Pharmacy, Cell Biology, Genomics and Proteomics, Pharmacogenomics, Bioinformatics and Biotechnology of Pharmaceutical Interest........more details on Aim & Scope).
Asymptomatic urinary tract infection amongst some Students of Michael Okpara ...Premier Publishers
This work was carried out to determine Asymptomatic Urinary Tract Infection amongst some students of Michael Okpara University of Agriculture, Umudike and the sensitivity pattern of the isolates from urine. Using aseptic technique, midstream urine were collected from sixty (60) students, urinalysis was carried out on the urine samples and was then cultured on CLED and MacConkey agar using pour plate method. Growth was observed in 26 (87%) of the sample while there was no growth in 4 (13%) of the sample. Out of the 26 (87%) samples with growth, 14 (47%) had significant bacteria growth while 12 (40%) had no significant growth. Incidence of asymptomatic bacteriuria was higher in females 8 (57%) than males 6 (38%). The organisms isolated were Escherichia coli, Klebsiella species, Staphylococcus saprophyticus, Staphylococcus aureus, Enterococcus faecalis, Proteus species, and Pseudomonas aeruginosa. All the Gram positive isolates were sensitive to Gentamycin and all resistance to Cefuroxime, Ceftazidime, Ceftriaxone, Cloxacillin. The Gram negative isolates were mostly sensitive to Nitrofurantoin, Gentamycin and Ofloxacin. Therefore, these drugs could be considered as the first line of drug for the treatment of asymptomatic urinary tract infection.
Background &Objective: Klebsiella pneumonia causes different serious nosocomial infections for human and several strains became multiple drug resistance .This study was conducted to describe the epidemiology and molecular typing of Klebsiella pneumonia with the extended spectrum of B lactamase enzyme in Gaza strip .Methods :A cross-sectional survey was conducted during the period of December 2008 to November2009. One hundred and fifty clinical specimens were collected from patients admitted in different wards . Results : Sixty six percentage of the isolates were K.pneumonia .These were isolated from different infected sites : urine 24% , sputum 14%, wound 11% , stool11% , blood14% , cerebrospinal fluid 11% , skin16% . The ESBLs was detected in 67% of the strains ,53% strains were resistant for more than eight antibiotics , PCR demonstrated different patterns for the presence of SHV(80%) , TEM(60%) enzyme and CTX-M(20%), PFGE Showed 10 clusters of genetically unrelated strains with high prevalence of polyclonal strains of Klebsiella pneumonia. Antibiotic resistance was found against Cephalothin(95.0%),Cefotaxime(82.0%),Ceftazidime(59.0%),Ceftriaxone(86.0%),Gentamicin(56.0%),Trimethoprim/sulphamethoxazole(47.0%)..Chloramphenicol(42%),Amikacin(33%),Aztreonam (32%) and Imipenem(0%). Interpretation, Conclusion : our findings showed that genetically-related isolates of K. pneumoniae producing SHV and TEM and CTX-M were present in Gaza Strip. Larger studies need to be done to better define the molecular epidemiology of ESBL producing K. pneumoniae and its clinical implications
Increase your Understanding of the Pathogenesis of Gluten Spectrum DisordersCell Science Systems
Recently, researchers at Harvard University, Alessio Fasano et. al., and the National Institutes of Health (laboratories of immunology and cellular and molecular biology), reported real-time microscopic observations of gluten-induced neutrophil activation.
According to authors, " To what extent neutrophil function adds to, or protects against, gluten intolerance is currently under vigorous investigation."
This presentation will shed light on this question. It will also review the Fasano study and examine the role of neutrophil function in multiple disease conditions, as well as explore how neutrophil function may also play a dual role in protecting the body from the untoward effects of dietary and environmental agents.
Abstract
Objective(s):
Abdominal adhesions are one of the most important problems, occurring after intra-abdominal surgery in more than 90% of cases. This condition is the leading cause of bowel obstruction, infertility, and abdominal/pelvic pain. Gold nanoparticles (GNPs) have been shown to be non-toxic and exhibit anti-inflammatory, anti-angiogenic and antioxidant activities. The purpose of this study was to determine the effect of intraperitoneal lavage with GNP solutions on the development of postoperative peritoneal adhesion (PPA).
Materials and Methods:
In the current experimental study, thirty-five male Wistar rats were randomly assigned to seven groups of five rats. After a standardized peritoneal injury, GNP solutions in different concentrations (1, 2.5, 5, 10, 50 and 100 ng/ml) were locally administered through nebulization; normal saline (NS) was administered to the control group. Two weeks later, the rats were sacrificed and cecum and peritoneal samples were harvested for histopathological assessment. Blood samples were obtained to determine serum concentrations of inflammatory biomarkers including tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β) and vascular endothelial growth factor (VEGF).
Results:
The rats treated with GNPs had significantly lower microscopic and macroscopic peritoneal adhesion scores, compared to the control group (P<0.05). Score 5 of macroscopic adhesions was reported in all the rats of the control group, unlike the GNP groups. Furthermore, microscopic adhesions were reported with all rats in the control group, unlike the GNP groups (reported in 0 out of 5 rats in all GNP groups). In addition, serum levels of IL-1β, TNF-α and VEGF underwent no significant changes.
Conclusion:
Compared to the control group, GNPs decreased the severity of peritoneal adhesions, although they did not alter TNF-α, IL-1β or VEGF serum levels.
Evaluation of pcr in the molecular diagnosis of trichomonas vaginalis infecti...Open Access Research Paper
Trichomonas vaginalis (T. vaginalis) is a common pathogen with worldwide distribution. It is estimated that worldwide 180 million people are infected annually. Trichomoniasis is associated with vaginitis, cervicitis, low birth weight, and preterm delivery. PCR has the advantage of high sensitivity, shorter time for diagnosis and the ability to detect nonviable or defective organism. In this study we used these three methods for evaluation of PCR in comparison with conventional methods like wet mount and culture in the detection of T. vaginalis in vaginal discharge. Three vaginal swab specimens were obtained from each of 200 cases, of the age group 18-40years, both symptomatic and asymptomatic females attending Gynaecology OPD(50) and Family planning OPD(50) at Gandhi hospital, Secunderabadand two FSW(Female sex workers) clinics (100) in highly concentrated areas of them in Hyderabad, for validation of various forms of Trichomonas vaginalis diagnostic procedures. One swab was immediately examined by wetmount microscopy, a second swab was placed in Wittington’s medium for cultivation, and other swab is placed in 2SP transport medium for PCR for T.vaginalis. A total of 58 samples positive in one or more tests were identified: 11 (5.5%) infections were detected by wet mount microscopy, and 30 (15%) positives in culture respectively. PCR was positive in 50 (25%) samples. PCR appears to be the most sensitive method with high detection rate and method of choice for detection of genital infections with T. vaginalis.
Structurally characterized arabinogalactan from Anoectochilus formosanus as a...Cây thuốc Việt
In this study, the innate immuno-modulatory effects and anti-cancer action of arabinogalactan (AG), a derivative of a well-known orchid, Anoectochilus formosanus, were investigated. The innate immunomodulatory effects of AG were determined in vitro using RAW 264.7 cells for microarray analysis, and in vivo using BALB/c mice administrated with AG at 5 and 15 mg/kg intra-peritoneally for 3 weeks. The anti-cancer activity of AG was evaluated by CT26 colon cancer-bearing BALB/c mice. The microarray
analysis was performed to evaluate the innate immunity and demonstrated that AG significantly induced the expression of cytokines, chemokines, and co-stimulatory receptors, such as IL-1, CXCL2, and CD69.
An intraperitoneal injection of AG in mice increased the spleen weight, but not the body weight. The treatment of mitogen, LPS significantly stimulated splenocyte proliferation in AG treated groups. The AG treatment also promoted splenocyte cytotoxicity against YAC-1 cells and increased the percentage
of CD3+CD8+ cytotoxic T cells in innate immunity test. Our experiments revealed that AG significantly decreased both tumour size and tumour weight. Besides, AG increased the percentage of DC, CD3+CD8+ T cells, CD49b+CD3− NK cells among splenocytes, and cytotoxicity activity in tumour-bearing mice. In addition, the immunohistochemistry of the tumour demonstrated that the AG treatments increased the tumour-filtrating NK and cytotoxic T-cell. These results demonstrated that AG, a polysaccharide derived
from a plant source, has potent innate immuno-modulatory and anti-cancer activity. AG may therefore be used for cancer immunotherapy.
Similar to The role of tumor necrosis factor final.for puplication (20)
2. stated that TNF-α played a pivotal role in induction, growth and metastasis of neoplasma. It can
induce phenotypic changes in gastric cells. Also, IFN-γ production by H. pylori causes peptic ulcer
and gastric inflammation (Holk 2003). These data confirmed the relation between the increased
cytokines and the inflammatory activity in gastric mucosa in H. pylori infection.
The aim of this study is to evaluate the magnitude of H pylori infection in patients with
gastritis and peptic ulcer by evaluating anti-H.pylori Ig G and Cag A positivity. Another aim is to
evaluate the role of TNF-α and IFN-γ as proinflammatory cytokines affecting the response to this
infection.
Patients and methods:
This work included 148 patients they were studied over 8 months at the outpatient clinic in
Theodor Bilharz research Institute and Agoza Hospital. Eighty six were males and 62 were
females with random age. Most of them complained from manifestations suggestive of upper
gastrointestinal diseases in addition to other extragastric manifestations such as; biliary and
chronic respiratory symptoms, general fatigue, bad odour of mouth, constipation and migraine.
All patients and controls were investigated for history and clinical examination, stool and urine
analysis, liver function tests, kidney function tests, abdominal ultrasound and upper
esophagogastroduodenoscopy. At least three gastric biopsies were taken (from anterior, posterior
walls of the antrum and the body of stomach) for histological assessment and H. pylori detection
(by direct microscopic examination and rapid urease test). They were also investigated for anti-H.
pylori Ig G. Patients with gastritis or peptic ulcers and positive H. pylori test by any methods were
investigated for Cag A positivity using ElISA technique and for TNF-α and IFN-γ levels in their
sera.
1- Detection of serum anti-H pylori Ig G:
Sera were collected from patient’s blood and specific anti-H pylori Ig G was assayed according
to Segal et al. (1996). Cultures were diluted 1:1000 and antigen was prepared by using the
sonicates from the H. pylori strain and protein content was estimated. Plates were coated with the
antigen and incubated over night at room temperature, then sera applied in dilutions of 1:200,
incubated for 1 hour at 370 C, then washed using PBS/T (pH 7.2), then the antihuman IgG
peroxidase conjugate (Sigma) was applied in a dilution of 1:1000 and incubated 30 minutes at
370 C, then washed 5 times with PBS/T and OPD substrate (Sigma) was then added, and the
reaction was stopped after 30 minutes using 8N H2SO4. optical density at 492 nm was identified.
2- Detection of Cag A:
A 66-Kda Cag A antigen fragment (Boehringes Mannheim Corp.) had been cloned in
Escherichia coli (PORV 220) as mentioned by Blaser et al. (1995). For the Cag A, ELISA were
coated with the previously prepared Cag A antigen and incubated over night at room
temperature. Plates were washed using PBS/T (pH 7.2) then patient’s sera diluted 1: 100 were
added and left for 1 hour at 370 C, then after wash, anti-human specific Ig G peroxidase
conjugate was added at 1:1000 dilution and left for 30 minutes at 370 C, then after wash, OPD
substrate was added and the reaction was stopped after 30 minutes and optical density was
measured at 492 nm. Cases with positive Cag A were proposed to TNF-α assay and IFN-γ
detection assay.
3- Detection of TNF- α :
Detection of TNF- α is done by sandwisch ELISA. TNF- α was assayed in patient's sera
according to Damas et al. (1989), using TNF-α enzyme immunoassay kit (Immunotech, A
coulter company, France). 100 μl of TNF- α conjugate was added to each well of microtitre
3. plate coated with anti-TNF- α standard, control and samples were added to all wells except the
blank and incubated for 120 minutes at room temperature with shaking. After washing 200 μl of
substrate were added to all wells including the blank well, then incubated for 30 minutes in the
dark at room temperature with shaking, the 50 μl of stop solution were added to all wells and
absorbance was read at 405 nm, the the concentration was calculated by interpolation from the
standard curve that was performed in the same assay.
4- Detection of IFN-γ by sandwisch ELISA:
IFN-γ was assayed in the sera of patients according to De Maeyer et al. (1992), using IFN-γ
enzyme immunoassay kit (Immunotech, A Beckman Coulter Company, France). A 96 microliter
plate applied with kit coated with anti- IFN-γ monoclonal antibody, 50 μl of standard or samples
were added to each well, plate was covered and incubated for 2 hours at room temperature with
shaking. After washing, 50 μl of biotinylated antibody, then 100 μl of streptavidin- HRP
conjugate were added to all wells, except to that for substrate blank and plate was incubated for
30 minutes at room temperature with shaking, then after washing 100 μl of TMB substrate was
added to all wells. Plate was incubated for 20 minutes at room temperature in the dark with
shaking, then 50 μl of stop solution were added to all wells and absorbance was read at 450 nm,
then the concentration was calculated by interpolation from the standard curve that was
performed in the same assay.
Statistical analysis:
The data was represented in mean of values ± SE using ANOVA (analysis of variance).
Results:
From the screening of GIT manifestations of 148 patients, 86 males and 62 females, it was
found that 71 males and 42 females suffered from different grades of gastritis as detected by gross
endoscopic examination and histopathology, while 13 males and 10 females had peptic ulcers
(with surrounding gastritis or duodenitis in all cases). Twenty eight subjects were considered as
negative controls with negative microbiological findings (negative urease test and negative
microscopic examination for H pylori and negative anti H. pylori IgG test). However, endoscopic
and histopathological findings of gastritis (in 4 cases) and peptic ulcers (in one case) were all
negative for H pylori by all means. They all have history of NSAID intake in the previous few
weeks. Tables 1 and 2 illustrate the number and percentage positivity of the controls and patients
infected with H. pylori (males and females) suffering from gastritis (gross and endoscopic) and
peptic ulcers. It includes also the results of rapid urease test done on gastric biopsies taken during
endoscopy. From the total patients of 148 showing microscopic gastritis, only 119 (80.4%) showed
gross gastritis by endoscopic examination and 23 (15.5%) showed gross peptic ulcer (18 duodenal
and 5 gastric ulcers). For males, 71 (48%) showed gross gastritis and 13 (8.8%) showed peptic
ulcers (11 duodenal and 2 gastric ulcers. For females, 48 (32.4 %) showed gross gastritis and 10
(6.8%) showed peptic ulcers (7 duodenal and 3 gastric ulcers). Males showed significantly higher
prevalence of microscopic gastritis than females (P<0.05) and insignificant differences for other
manifestations. H. pylori organism was detected in 133 cases (89.9%), while rapid urease test was
positive in (126 (85.1%) of total cases using antral biopsies. These results showed that microscopic
examination of gastric biopsy is more sensitive than urease test for detection of H. pylori.
Table 3 shows the anti-H. pylori antibody and Cag A positivity in different cases and sex
distribution. Antibody positivity was found in 91.5 % of male patients and in 81.25 % of female
patients with gastritis. In patients with peptic ulcers, antibody positivity was found in 76.9 % in
males and in 70 % in females. Cag A positivity was detected in 87.3 % of males and in 75 % of
females with gastritis. It was detected in 61.5 % of males and in 60 % of females with peptic
4. ulcers. H pylori and Cag A positivity were significantly higher among male patients than females
with gross gastritis (P<0.05).
Table 4 shows the results of TNF- α and IFN-γ levels in patients and control group. In controls,
the mean TNF- α level was 301±112 Pg/ml while it was 448±257 Pg/ml for males and 352±231
Pg/ml for females with gastritis. In peptic ulcer patients, it was 498±305 Pg/ml for males and
568±341 Pg/ml for females. It was significantly higher in all types of patients than in controls (P<
0.01). The mean IFN-γ level in controls was 0.41 ± 0.23 IU/ml. It was 0.73±0.42IU/ml for males
and 0..56±0.51IU/ml for females with gastritis. In peptic ulcer patients, it was 0.61 ±0.32 IU for
males and 0.82 ±0.37 IU for females. It was also significantly higher in all types of patients than in
controls (P< 0.01). Only TNF- α was significantly higher in males than females with gastritis (P
<0.01) but not with peptic ulcer and not for IFN-γ (P>0. 05).
Table 1: endoscopic, microscopic and urease test findings in controls and patients of this study.
Number Gross findings Microscopic examination. Urease Test
gastritis Peptic U. gastritis H. pylori positivity positivity
Controls 28 2 1 4 0 0
Total patients 148 119
(80.4%)
23 148 133
(89.9%)
126
(85.1%)
Males 86 71 13 86* 81 76
Females 62 48 10 48 52 50
* Males showed significantly higher prevalence of microscopic gastritis only than females (P<0.05).
Table 2: summary of table 1.
Patients Total Number Gastritis (gross) Peptic ulcers
Number Percentage Number Percentage Number Percentage
Total 148 100 % 119 80.4 % 23 15.5 %
Males 86 58.1 % 71 48 % 13 8.8 %
Females 62 41.9 % 48 32.4 % 10 6.8 %
Table 3: anti-H. pylori antibody and Cag A positivity in different cases and sex distribution
Patients Total
number
Percentage of anti-H. pylori
positivity
Percentage of Cag A
positivity
Number of cases % Number of cases %
gastritis Males 71 65 91.5 % * 62 87.3 %*
Females 48 39 81.25 % 36 75 %
peptic
ulcer
Males 13 10 76.9 % 9 61.5 %
Females 10 7 70 % 6 60 %
* H pylori and Cag A positivity were significantly higher among male patients than females
with gross gastritis (P<0.05).
Table 4: TNF- α and IFN-γ in patients and control group
Number TNF- α IFN-γ
Control 28 301 ±112 Pg/ml 0.41 ± 0.23 IU/ml
Patients Gastritis Peptic ulcers
No. TNF- α IFN-γ No. TNF- α IFN-γ
Males 65 448±257 Pg/ml 0.73±0.42IU/ml 10 498±305 Pg/ml 0.61 ±0.32 IU
Females 39 352±231 Pg/ml 0..56±0.51IU/ml 7 568±341 Pg/ml 0..82 ±0.37 IU
*Both TNF- α and IFN-γ levels were also significantly higher in all types of patients than in controls
(P< 0.001). Only TNF- α was significantly higher in males than females with gastritis (P <0.01)
but not with peptic ulcer and not for IFN-γ (P>0. 05).
6. Atrophic gastritis is characterized by glandular atrophy and likely represents a precursor state
for gastric adenocarcinoma (Correa 1992). Nonneoplastic mucosa adjacent to gastric carcinomas
and lymphomas often displays atrophy, dysplasia, and intestinal metaplasia (Arista-Nasr et al.,
2001). H. pylori organisms rarely are observed in association with regions of atrophic gastritis or
gastric adenocarcinoma. A second form of gastric neoplasia, gastric MALT lymphoma, may be
evaluated by histopathologic studies. Gastric marginal zone B-cell lymphomas (or MALT
lymphomas) are highlighted histologically by the presence of lymphoepithelial lesions, prominent
lymphoid follicles, and extensive zones of marginal B lymphocytes infiltrating the mucosa
(Isaacson 1994). H pylori organisms may be visualized adjacent to areas of low-grade gastric
MALT lymphomas but are observed less commonly in association with diffuse large B-cell
lymphomas (high-grade MALT lymphomas).
In the present study, type 1 bacteria with Cag A positivity were significantly higher (P < 0.05)
in patients with both diseases of H. pylori. It was detected in 87.3% of male patients and in 75% of
female patients with gastritis and in 61.5% of males and in 60% of females with peptic ulcers.
These results were in accordance with that of Gasbarrini et al., (1997). It was found that H pylori
type 1 caused more severe illness and other associated diseases (Sozzi et al., 1998; Rudi et al.,
2000 and Kato et al., 2000). Gasbarrini et al., (1997) studied and discussed the association of Cag
A positivity with abdominal and extra-abdominal manifestations. He found that 11 out of 15
patients with peptic ulcers, were Cag A positive which is statistically significant.
In our study, anti-H pylori Ig G antibody was detected in 91.5% of males and in 81.25% of
females with gastritis while in patients with peptic ulcers, it was detected in 76.9% in males and in
70% in females. A previous study showed that antibodies to H. pylori infection were present in
64.5 % of infected patients (Durazzo, 2002). In another study, Gasbarrini et al., (1999) found a
prevalence of anti H. pylori antibodies of 77 % in patients with cirrhosis due to HCV infection and
in 59 % in matched blood donors.
Most patients infected with H pylori produce a measurable systemic immune response,
composed primarily of IgG (Rathbone et al.,1986 and Perez-Perez et al., 1988). Serum IgA may be
detected in fewer than half (range, 39%-82%) of infected patients, and serum IgM is found rarely.
Since few patients have been evaluated during the acute phase of infection, data about the nature of
the acute antibody response and seroconversion from IgM to IgG are sparse. Seroconversion to
IgG was demonstrated between 22 and 33 days after infection in one volunteer study (Morris and
Nicholson 1987). In naturally acquired infection, an initial serum IgM response was observed, and
seroconversion of IgM to IgA was documented. Circulating anti-H pylori IgG antibodies persist at
constant levels for years during infection. Levels of IgG1, IgG2, and IgG4 subclasses typically are
elevated, whereas IgG3 antibodies (associated with acute infections) are not detected (Sobala et al.,
1991). Autoimmune and corpus-predominant atrophic gastritis have many overlapping features.
Antigastric antibodies are generated in a subset of infected individuals and include antiluminal and
anticanalicular antibodies. A principal target of H pylori-associated autoantibodies is the parietal
cell proton pump, H+,K+-ATPase (Claeys et al., 1998).
The key pathophysiologic event in H. pylori infection is the initiation of an inflammatory
response (Israel et al., 2001). This response is most probably triggered by the bacterium's
lipopolysaccharide, urease, and/or cytotoxins and is mediated by cytokines. The cytokine
repertoire comprises a multitude of pro- and anti-inflammatory mediators whose function is to co-ordinate
an effective immune/inflammatory response against invading pathogens without causing
undue damage to the host. In addition to their pro- or anti-inflammatory properties, some H.
pylori-induced cytokines have direct effects on gastric epithelial cells that have a profound effect
7. on gastric physiology. For example, the pro-inflammatory cytokine interleukin-1 beta (IL-1beta )
is the most potent of known agents that are gastric cytoprotective, antiulcer, antisecretory, and
inhibitors of gastric emptying (Robert et al., 1991 and Wolfe and Nompleggi, 1992). Another
important pro-inflammatory cytokine that is up-regulated by H. pylori infection is tumor necrosis
factor alpha (TNF-alpha ), which also inhibits gastric acid secretion, but to a lesser extent than IL-
1beta (Beales and Calam, 1998). Cytokines appear to regulate the migration of Th 1 and Th 2
lymphocytes to inflamed tissues during the immune response. A dual effect of H. pylori on the Th
1 response was verified. A stimulation response was verified by increase of IFN-γ and TNF-α
(berribi et al., 2003 and Holk,2003). These studies confirmed the connection between increase of
IFN-γ and TNF-α and the inflammatory activity in gastric mucosa due H. pylori infection. A
significant increase of IFN-γ and TNF-α levels in the sera of patients infected with H. pylori has
been reported by Tsuji et al (2003), Konturk et al. (2003) and Slomiany (2003). In the present
study, a highly significant increase of TNF-α levels (P<0.01) was detected in both males and
females with gastritis and peptic ulcer. Also a significant increase of IFN-γ levels (P<0.01) was
detected in both males and females with gastritis and peptic ulcer due to H. pylori infection. These
results are in accordance with the results obtained by Holk (2003), Tsuji (2003), Konturk et al.
(2003) and Slomiany (2003). In one study, it was found that the severity of gastritis associated
with H pylori infection was correlated with mucosal expression of the tumor necrosis factor alpha
subunit and IFN-gamma (Lehmann , et al. 2002)
In this study, classification of patients according sex showed some differences in the
manifestations and blood tests among both males and females. Males showed significantly higher
prevalence of microscopic gastritis than females (P<0.05). There was no difference among both
sexes as regards to peptic ulcer which might be due to small number of cases. H pylori and Cag A
positivity were significantly higher among male patients than females with gross gastritis (P<0.05).
Only TNF- α was significantly higher in males than females with gastritis (P <0.01) but not with
peptic ulcer and not for IFN-γ (P>0. 05). Previous studies showed also that the prevalence of
peptic ulcer was shifted from being a disease predominant in males to one with a nearly
comparable prevalence in both sexes and nearly at the same age (Kurata et al.,1986 and Turkdoan
et al., 1999). However, the incidence and male to female ratio still increased with advancing age
(Mowaten et al., 1975).
From the present study, it was concluded that H. pylori is the main cause of gastritis and peptic
ulcer and the disease was caused mainly by type 1 bacterium as obtained by the detection of Cag A
positivity. Also, it seems from this study that Cag A positivity can be used as an additive
diagnostic marker to other methods of diagnosis. It could be also concluded that evaluation of IFN-
γ and TNF-α levels might play a role in the diagnosis and prognosis of H. pylori infection. In this
study, there were sex predilection of some manifestations, particularly microscopic gastritis, and
Cag A positivity which were more in males than females.
دور عامل التأكل الورمى ألفا والنتترفيرون جاما كسيتوكينات مسببة لللتهاب فى حالت التهاب المعععدة
والقرح الهضمية الناتجعة ععن الصاعابة بالبكتريعا الحلزونتيعة البوابيعة وتقييعم الجسعام المضعادة ج وال
كوسائل تشخيصية مناعية فى النتسان. Cag A
شندى محمد شندى*، نتهال العسالى**، هناء منصور*** و وفاء منصور***
معهد تيودور بلهارس للبحاث، قسم الجهعاز الهضعمى والكبعد والمعراض المتوطنعة *و قسعم الكيميعاء الكلينيكيعة و**
و*** قسم المناعة هناء منصور، شندى محمد شندى، وفاء منصور و نتهال العسالى
8. ان البكتريععا الحلزونتيععة البوابيععة هععى سععبب مهععم للكععثير مععن العععراض الهضععمية والغيععر هضععمية وإنتهععا تحفععز تكععوين
السيتوكينات المسببة لللتهابات وتكوين الجذور الحرة. كم ان التهاب المعدة والقرح الهضمية غالبا ما يصاحبها ارتفععاع
فى التعبير عن عامل التأكل الورمى ألفا والنتترفيرون جاما.
وكان الهدف من هعذه الدراسعة هعو تقييعم دور عامعل التأكعل العورمى ألفعا والنتعترفيرون جامعا كمسعببات لللتهابعات فعى
المرضى المصابين بالبكتريا الحلزونتية البوابية وقياس الجسام المضادة ج فى دم المرضى وعمععل ربععط بيععن ايجابيععة ال
وبين التهاب المعدة والقرح الهضمية . Cag A
وقد شملت هذه الدراسة ١٤٨ مريضا ( ٨٦ رجل و ٦۲ أنتثى) و ۲٨ حالة سليمة للمقارنتة. وتم عمل فحص شامل لجميععع
كما تم قياس عامل التأكل الورمى ألفععا والنتععترفيرون ELISA بطريقة Cag A المرضى وعمل الجسام المضادة وال
و قد أظهرت النتائج أنته فى حالة التهاب المعععدة فعان ايجابيعة الجسعام المضعادة .Cag A جاما فى المرضى ايجابي ال
فى الذكور ٣,٨٧ % وفى النتاث ٧٥ % أما فى Cag A كانتت فى الذكور ٥,٩١ % وفى النتاث ۲٥,٨١ % وايجابية ال
Cag حالت القرحة الهضمية فقد كانتت ايجابية الجسام المضادة فى العذكور ٩,٧٦ % وفعى النتعاث ٧٠ % وايجابيعة ال
فى الذكور ۲,٦٩ % وفى النتاث ٧٠ %. وقد كان مستوى عامل التأكل الورمى ألفا والنتعترفيرون جامعا أعلعى علعوا A
ذو دللة فى المرضى عنهما فى حالت المقارنتة.
يستنتج من هذا البحث أنته من المهم دراسة السيتوكينات ودورها فى اللتهابات الناتجة عن الصاابة بالبكتريعا الحلزونتيعة
فعى Cag A البوابية فى مرضى التهاب المعدة والقرح الهضمية، كما يستنتج أيضا أن قيععاس الجسعام المضععادة ج وال
هؤلء المرضى أعطى دللت مناعية تشخيصية جيدة قبل عمل المنظار المعدى.
References:
1. Arista-Nasr J, Jimenez-Rosas F, Uribe-Uribe N, et al. (2001): Pathological disorders of the gastric mucosa
surrounding carcinomas and primary lymphomas. Am J Gastroenterol.; 96:1746-1750.
2. Beales IL, Calam J. (1998): Interleukin 1 beta and tumour necrosis factor alpha inhibit acid secretion in
cultured rabbit parietal cells by multiple pathways. Gut ; 42(2): 227-234.
3. Berrebi D.; Languepin J.; Ferkdaji L.; Foussat A.; De Lagausie P.; Paris R.; Emilie D.; Mongenot J.F.;
Cezard J.P.; Navarro J. and Peuchmaur M. (2003): Cytokines, Chemokines, receptors and homing
molecules distribution in the rectum and stomach of paediatric patients with active ulcerative colitis. J.
parasitol. Gastroenterol. Nutr., 37 (3): 300-8.
4. Blaser M. J.; Perez-Perez G. I.; Kleahous H.; Cover T. L.; Peek P.M.; Chyous P. H.; Stemmemann G. N.
and Nomura A. (1995): Infection with helicobacter pylori strains possessing Cag Associated with an
increased risk of developing adenocarcinoma of the stomach. Cancer Res., 55: 2111-2115
5. Claeys D, Faller G, Appelmelk BJ, et al. (1988): The gastric H+,K+-ATPase is a major autoantigen in
chronic Helicobacter pylori gastritis with body mucosa atrophy. Gastroenterology ; 115:`340-347.
6. Correa P. (1992): Human gastric carcinogenesis: a multistep and multifactorial process: First American
Cancer Society Award Lecture on Cancer Epidemiology and Prevention. Cancer Res. ;52:6735-6740
7. Damas P.; Peuter A.; Gysen P.; Demonty J.; Lamy M. and Franchimont P. (1989): Tumor necrosis factor
and Interleukin 1 serum levels during severe sepsis in human. Crit. Care Med. 17: 975-983.
8. David Y and Graham M.D. (2000): H. pylori. Helicobacter; 5(suppl. 1): 3-31.
9. De Maeyer E. and De Maeyer G.I. (1992): Interferon gamma. Curr. Opinion Immunol.; 4:321-332.
10. Durazzo M.; Pellicano R.; Premoli A.; Berrutti M.; Leone N.; Ponzetto A. and Rizzetto M. (2002):
Helicobacter pylori seroprevalence in patients with autoimmune hepatitis. Dig. Dis. Sci.; Feb: 47 (2): 380-
383 .
11. Faller G., Kirchner T.(2001): Helicobacter pylori and antigastric autoimmunity [in German]. Pathologe.;
22:25-30.
12. Gasbarrini A.; De Luca A.; Fiore G.; Ojetti V.; Franceschi F.; Candelli M.; Torre E.S.; Gasbarrini G.;
Campli C. and Massari I., (1997): Helicobacter pylori and primary headache. Gastroenterol. Int. 10 (suppl)
13.
13. Gasbarrini A.; Franceschi F.; Armuzzi A.; Ojetti V.; Candelli M.; Torre E.S.; Gasbarrini G. (1999):
Extradigestive manifestations of Helicobacter gastritis infection. Gut, Jul; 45 suppl. 1: 91-112.
9. 14. Greenberg PD, Koch J, Cello JP.(1996): Clinical utility and cost effectiveness of Helicobacter pylori testing
for patients with duodenal and gastric ulcers. Am J Gastroenterol. ;91:228-232.
15. Holck S.; Norgaard A.; Bennedsen M.; Permin H.; Norn S. And Anderson L. (2003): gastric mucosal
cytokine response in Helicobacter pylori infected patients with gastritis and peptic ulcers. Association with
inflammatory parametersand bacterial load. Immunol. Med. Microbiol., 36 (3):175-180.
16. Israel DA, Peek RM.(2001): pathogenesis of Helicobacter pylori-induced gastric inflammation. Aliment
Pharmacol Ther; 15(9): 1271-1290.
17. Kato S.; Onda M.; Yamada S.; Matsuda N.; Tokunaga A.; and matsukura N. (2000): Association of the
interleukin-1 beta genetic polymorphism and gastric cancer risk. Japanese J. Gastroenterol., Oct; 36 (10):
696-699.
18. Konturek P.C.; Kania J.; Konturek J.W.; Nikiforuk A.; Konturek S.J. and Halhn E.G. (2003): H. pylori
infection, atrophic gastritis, cytokines, gastrin, COX-2, PPAR-gamma and impaired apoptosis in gastric
carcinogenesis. Med. Sci. Monit., 9 (7): 5366.
19. Kuipers EJ.(1997): Helicobacter pylori and the risk and management of associated diseases: gastritis, ulcer
disease, atrophic gastritis and gastric cancer. Aliment Pharmacol Ther. 1997;11(suppl 1):71-88.
20. Kurata J H, Elashoff J D, Nogawa A N and Haile B M (1986): Sex and smoking differences in
duodenal ulcer mortality. American Journal of Public Health, Vol. 76, Issue 6 700-702
21. Mowatn N. A. G., Needham C. D and Brunt P. W. (1975): The Natural History of Gastric Ulcer in
a Community: A Four-year Study Q J Med 1975; 44: 45-56
22. Morris A, Nicholson G.(1987): Ingestion of Campylobacter pyloridis causes gastritis and raised fasting
gastric pH. Am J Gastroenterol.; 82:192-199.
23. Parsonnet J.; Blaser M. J.; Perez-Perez G.I.; Hargrett-Bean N. And Tauxe R.V. (1992): Symptoms and risk
factors of Helicobacter pylori infection in a cohort of epidemiologists. Gastroenterology, 102: 41-46
[Medline].
24. Peek P.M. and Blaser M.J. (2000): Helicobacter pylori and gastrointestinal tract adenocarcinomas. Nat.
Rev. Cancer, Jan; 2 (1): 28-37.
25. Perez-Perez G.I; Peek R.M.; Legath A.J.; Heine P.R. and Graff L.B. (1999): The role of Cag A status in
gastric and extragastric complications of Helicobacter pylori. J. Physiol. Pharmacol., Dec.: 50 (5): 833-45.
26. Perez-Perez GI, Dworkin BM, Chodos JE, et al.(1988): Campylobacter pyloriantibodies in humans. Ann
Intern Med. 1988;109:11-17.
27. Rathbone BJ, Wyatt JI, Worsley BW, et al.(1986): Systemic and local antibody responses to gastric
Campylobacter pyloridis in non-ulcer dyspepsia. Gut.; 27:642-647.
28. Robert A, Olafsson AS, Lancaster C, Zhang WR.(1991): lnterleukin-1 is cytoprotective, antisecretory,
stimulates PGE2 synthesis by the stomach, and retards gastric emptying. Life Sd; 48(2): 123-134.
29. Rubin CE.(1997):Are there three types of Helicobacter pylori gastritis? Gastroenterology.; 112:2108-
2110.
30. Rudi J.; Reuther S.; Sieg A.; Hoerner M. And Stremmel W. (2000): Relevance of underlying disease and
bacterial Vac A and Cag A status on the efficacy of Helicobacter pylori eradication. Digestion, 65 (1):15.
31. Segal Segal E.D.; Falkow S. and Tompkins L.S. (1996): Helicobacter pylori attachment to gastric cells
induces cytoskeletal rearrangements and tyrosine phosphorylation of host cell proteins. Proc. Nat. Acad.
Sci. USA, 93: 1259-1264.
32. Sepulveda A.R. and Coelho L.G. (2002): Helicobacter pylori and gastric malignancies. Helicobacter, 7
(suppl) 1: 37-42.
33. Sharma P, Topalovski M, Mayo MS, et al. (2000): Helicobacter pylori eradication dramatically improves
inflammation in the gastric cardia. Am J Gastroenterol.; 95:3107-3111
34. Sobala GM, Crabtree JE, Dixon MF, et al. (1991): Acute Helicobacter pylori infection: clinical features,
local and systemic immune response, gastric mucosal histology, and gastric juice ascorbic acid
concentrations. Gut; 32:1415-1418.
35. Solimany B.L. and Solimany A. (2003): Platelet activating factor modulates gastric mucosal inflammatory
response to Helicobacter pylori lipopolysaccharide. Biochem. Biophys. Res. Commun., 306 (1): 261-266.
36. Sozzi M.; Valentini M.; Figura N.; De Paoli P.; Tedeschi R.M.; Gloghini A.; Serraino D.; Poletti M. and
Carbone A. (1998): Atrophic gastritis and intestinal metaplasia in Helicobacter pylori infection: the role of
Cag A status. Am. J. Gastroenterol., Mar; 93 (3): 375.
10. 37. Tsuji S.; Kawai N.; Tsuji M.; Kawano S. Hori M. (2003): review article: Inflammation-related promotion
of gastrointestinal carcinogenesis; a perigenetic pathway. Aliment. Pharmacol. Ther.,18 (1): 82-89.
38. Turkdoan M.K., Hek M H., Tuncer I, Aksoy H (1999): The epidemiological and endoscopic
aspects of peptic ulcer disease in Van region. Eastern Journal of Medicine 4 (1): 6-9, 1999.
39. Wedi B. and Kapp A. (2000): Helicobacter pylori infection in skin diseases: a critical appraisal. Am. J.
Clin. Dermatol.; 4: 273-282.
40. Wolfe MM, Nompleggi DJ. (1992): Cytokine inhibition of gastric acid secretion - a little goes a long way.
Gastroenterology; 102(6): 2177-2178.
41. Xiang Z.; Cencini S.; Bayeli P.F.; Telford J.L.; Figura N.; Rappuoli R. and Covacci A. (1995): Analysis of
expression of Cag A and Vac A virulent factors in 43 strains of H. pylori. Infect. Immun. , 36: 94-98.
42. Yuhong Yuan; Ireneusz T Padol; Richard H Hunt (2006): Peptic Ulcer Disease Today. Nat
Clin Pract Gastroenterol Hepatol. 2006;3(2):80-89.
43. Zucca E.; Roggero E.; Maggi-Solea N.; Conconi A.; Bertoni F.; Reilly I.; Castelli D.; Pedrinis E.; Pifffaretti
J.C. and Cavalli F. (2000): Prevalence of Helicobacter pylori and Hepatitis C virus infection among non-
Hodgkin’s lymphoma patients. Southern Switzerland Haematologica, Feb: 85 (2): 147-153.
160 patients with gastritis and peptic ulcers
total patients gastritis peptic ulcer
140
120
100
80
60
40
20
0
females males total patients
Figure 1: Number of patients with gastritis and peptic ulcer (according sex).
11. 80
70
60
50
40
30
20
10
0
total gastritis
patients
Ig G positive Cag A positive
males with gastritis females with gastritis
Figure 2: anti-H. pylori antibody and Cag A positivity in male and female patients with gastritis
14
12
10
8
6
4
2
0
Anti-H. Pylori and Cag A positivity in Patients with peptic
ulcers
total patients anti H.pylori+ Cag A+
males
females
Figure 3: anti-H. pylori antibody and Cag A positivity in male and female patients with p. ulcer.
12. TNF in controls and patients with gastritis and peptic ulcer
600
500
400
300
200
100
0
1 2
females, males
Control gastritis peptic ulcer
Figure 4: TNF-α in controls and patients with gastritis and peptic ulcers.
0.9
0.8
0.7
0.6
0.5
0.4
0.3
0.2
0.1
0
IFN in controls and patients with gastritis and peptic ulcers
1 2
females, males
controls males females
Figure 5: IFN-γ in controls and patients with gastritis and peptic ulcers.