The document discusses the role of inflammation and macrophages in chronic illnesses, asserting that inflammation dysregulation underlies diseases such as cancer, heart disease, and autoimmune disorders. It highlights macrophage functions, including their transformation into foam cells and tumor-associated macrophages, and how these processes contribute to disease progression. The document also explores potential treatment strategies, including the use of dietary flavonoids and natural products for managing inflammation-related disorders.

1. The I Factor -
Inflammation, Immunity,
Illness
Presented by
Dr William Barnes, BSc, MB ChB

2. • Healing is a Personal Journey
• Science and Healing
• Science and Theory
• Science and Observation

3. Outline
• Background
• Immunity and Inflammation
• Inflammation and Macrophages
• Macrophage Pathology
• Foam Cell, Viruses, TAMs
• The Brune Theory & Nitric Oxide
• Macrophages in Disease States
– Treatment Strategies
• Colds and Influenza
– Treatment Strategies

4. Immunity and Inflammation

5. Immunity and Inflammation
• Inflammational dysregulation is at the root
or all chronic illnesses.
– Cancer, heart disease, arthritis, asthma,
bronchitis, Alzheimer’s disease,
schizophrenia, multiple sclerosis, etc.

6. Abnormal Immunity
• Innate immune system becomes
dysfunctional and perpetuates the disease
process.

7. The Innate Immune System in
Action

8. Components of the
Immune System

9. Omega-6 and Omega-3
Conversion Pathways

10. Macrophages

12. Macrophages
• Makros (large) + phagein (eat) = big eaters.
• Monocytes enter damaged tissue through the
endothelium of a blood vessel and undergoes
transformation to a macrophage.
• Monocytes are attracted to the site by chemotaxis,
triggered by a range of stimuli including damaged
cells, pathogens and cytokines released by
macrophages already at the site. They can survive
up to several months.

13. Fixed Macrophages
• Alveolar
macrophages
• Histiocytes
• Kupffer cells
• Microglia
• Epithelioid
• Osteoclasts
• Sinusoidal lining
cells
• Mesangial cells
• Lungs
• Connective tissue
• Liver
• Neural tissue
• Granulomas
• Bone
• Spleen
• Kidney

14. Phagocytosis

15. Macrophage Activation
TNF-α
LPS
NO

16. Nitric Oxide Synthesis
Citrulline
Ornithine
NO
Urea
Arginase
Nitric Oxide Synthase
(NOS)Arginine

17. Nitric Oxide
• Two main types:
- iNOS (inducible nitric oxide synthase),
produced by macrophages
- eNOS (endothelial nitric oxide synthase),
responsible for endothelial dilatation.

18. Macrophages and Disease
• Macrophages called foam cells may be
predominant in the pathogenesis of
atherosclerosis.
• Macrophages play a role in HIV, they become
infected and then become incubators for the
human immunodeficiency virus.
• Macrophages called TAMs (tumour associated
macrophages) are associated with cancer
proliferation and spread partially by activation of
NFkB activation and the inhibition of apoptosis,
and also through production of TNF-α.

19. Macrophages
• Environmental oestrogens promote IL-1β activity
in macrophages.
• Genistein and certain xeno-oestrogens
synergised with LPS to activate IL-1β promoter
activity. Environmental oestrogens have agonist
activity both on reproductive tissue along with
haemopoietic tissue.
– Endocrine 1998 Oct;9(2):207-11.

20. Foam Cells
• In the arterial intima, monocytes are transformed
into macrophages which then proceed to ingest
oxidised LDL.
• This foam cell transformation alters the phagocytic
and antimicrobial function of the macrophage and
may well allow the documented associated
infection with microbes, such as chlamydia
pneumonia, within the atherosclerotic plaques.
• Cholesterol accumulation by macrophages impairs
phagosome maturation.
– J Biol Chem. 2008 Dec 19;283(51):35745-55.

21. Flavonoids and
Endothelial Health
• Dietary flavonoids reduce oxidised LDL in
endothelial cells.
• Endothelial apoptosis is a driving force in
the development of atherosclerosis.
• EGCG, hesperetin and quercetin decrease
the influence of LDL signalling on the
induction of apoptosis.
– J Nutr. 2008 Jun;138(6):983-90.

22. TAMs
• Tumour associated macrophages are
obligate partners for malignant cell
migration, invasion and metastasis.
• The more TAMs the worse the prognosis.
– J Exp Med. 2001 Mar 19;193(6):727-40.

23. TAMs Effectors of Angiogenesis
and Tumour Progression
• TAMs are a prominent inflammatory cell
population in many tumour types residing in both
perivascular and avascular, hypoxic regions of
these tissues.
• Analysis of TAMs in human tumour biopsies has
shown they express a variety of tumour promoting
factors and the evidence from transgenic murine
tumour models has provided unequivocal
evidence for the importance of these cells in
driving angiogenesis, lymphangiogenesis,
immunosuppression and metastasis.
– Biochim Biophys Acta. 2009 Mar 6.

24. The Brune Theory
• Macrophages phagocytose apoptotic cells (AC).
• Phagocytosis of AC regulates the immune response by
shifting the phenotype of the macrophage to an anti-
inflammatory type (M2).
• AC in the M2 macrophage enhances the expression of
arginase II; this halts the induction of NO formation in
IFN-gamma stimulated macrophages.
• AC triggers IL-10, TGF-β, PGE2 production; reduced
capacity to produce TNF-α.
• TAMs support tumour growth survival and contibute to
angiogenesis and immune evasion.
– Mol Biol Cell. 2007 Oct;18(10):3810-9.

25. Brune Theory - M2 Macrophage
Citrulline
Ornithine
NO
Urea
Arginase
Nitric Oxide Synthase
(NOS)Arginine

26. Carnitine
• Carnitine decreases arginase activity.
• High levels of arginase and ornithine in different
carcinomas may indicate their relation to cancer.
• Carnitine is a cofactor required for the
transformation of free long-chain fatty acids into
acetylcarnitines. Carnitine may have an effect on
the ornithine arginase tissue levels.
• Conclusion: NO levels were significantly higher
in the carnitine treated group whilst the tissue
level of arginase activity and ornithine was
significantly decreased.
– Cell Biol Int. 2007 Nov;31(11):1414-9.

27. Effect of Carnitine on
Nitric Oxide Synthesis
Citrulline
Ornithine
NO
Urea
Arginase
Nitric Oxide Synthase
(NOS)Arginine
Carnitine

28. Macrophages and
Helicobacter pylori
• Macrophages and Helicobacter pylori infection
lead to gastric cancer.
• Gastric infection by H. pylori extract (HPE)
activates the production of cytokines and
chemokines by mononuclear cells.
• IL-8 is one of the major HPE triggered cytokines.
• This is activated by HPE mediated LPS
stimulation of macrophages; also amplifies the
inflammatory response.

29. Characteristics of Inflammatory
Infiltrate of Gastric Mucosa in Patients
with Dysplasia and Cancer
• 85 patients.
• Composition of the inflammatory infiltrate from gastric
mucosa (GM) was determined.
• Patients with adenocarcinoma showed an increase in
lymphocytes, neutrophils and macrophages.
– Klin Med (Mosk). 2008;86(11):48-53.

30. • Helicobacter pylori infection results in neutrophil
activation and chronic gastritis, and this has a
role in the development of gastric cancer.
• The greater the intensity of HPE infection, the
greater the degree of neutrophil activation and,
in turn, the gastritis and metaplasia.
– Niger J Clin Pract. 2008 Sep;11(3):270-4.
Characteristics of Inflammatory Infiltrate
of Gastric Mucosa in Patients with
Dysplasia and Cancer

31. Idiopathic Pulmonary Fibrosis
(IPF)
• IPF is a chronic, progressive, and often fatal lung
disease of unknown aetiology.
• Characterised by onset of infiltrate in the parenchyma of
the lung tissue.
• This infiltrate has been identified as lymphatic
endothelial cells (LECs).
– Proc Natl Acad Sci U S A. 2009 Mar 10;106(10):3958-63.
• Alveolar regions of the lung are usually devoid of LECs.
– Alveolar macrophages either promote the transformation of
lymphocytes into LECs, OR
– Macrophages themselves become LECs and form the basis for
this granulation tissue.

32. MMPs
• MMPs (Matrix metalloproteinases) are a family of
enzymes involved in the breakdown of extracellular
matrix in normal physiological processes such as
embryonic development, reproduction (endothelial
menstrual breakdown) and tissue remodelling.
• They are activated in diseases such as arthritis,
cancer metastasis and pulmonary fibrosis.
• LPS activated macrophages produce TNF and NO
which in turn activate MMPs.
• MMP-2 and MMP-9 are two of particular interest in
diseases.

33. Arthritis
33

34. Arthritis and the
Immune System

35. Natural Products - A Gold Mine
for Arthritis Treatment
• Study conclusions:
– Although various treatments for arthritis exist they
suffer from various drawbacks such as lack of
efficacy, excessive side effects and high cost.
– Arthritis requires a lifetime of treatment.
– Plant-derived products offer promise but require
investigation, however owing to the lack of
intellectual property rights, the pharmaceutical
industry has little motivation to pursue the
studies.

36. • Potential treatment strategies for arthritis:
– Suppress the expression of:
• TNF-α,
• IL-1β,
• COX-2,
• LOX,
• MMPs.
– Suppress NFkB.
• Curcumin, resveratrol, boswellic acids,
quercetin, tea polyphenols, etc.
– Curr Opin Pharmacol 2007 Jun;7(3):344-51.
Natural Products - A Gold Mine
for Arthritis Treatment

37. Curr Opin Pharmacol. 2007 Jun;7(3):344-51.

38. Synergy
• Different polyphenol herbs have slightly different
actions on different survival pathways.
• Quercetin on its own only starts its action at
10mM.
– Quercetin action is mediated through reduction of
iNOS, TNF-α, or LOX.
– Synergy between green tea and curcumin or
resveratrol will bring stronger influence on other
pathways such as Akt inhibition where these other
herbs have shown greater effect. Curcumin for
instance is a stronger inhibitor of the COX pathway.
• This synergy will also be of effect in other
inflammatory conditions and with pain in general.

39. Flavonoids

40. Flavonoids
• High intake of dietary isoflavones is linked
to the inhibition of COX activity in human
macrophages.
– Nutr Cancer. 2004:49(1):89-93.

41. Flavonoids
• Inhibition of iNOS and COX-2 expression by flavonoids
in macrophages.
• Flavonoids quercetin, galangin, apigenin and naringenin
markedly decreased PGE2 and COX-2 expression in a
concentration dependent manner.
• The same flavonoids modulated the expression of iNOS
between 5-50μM.
– Achievable with 1500mg quercetin orally.
– Life Sci. 2001 Jan 12;68(8):921-31.

42. Flavonoids
• Flavonoids affect oral anti-inflammatory activity
and inhibit systemic TNF-α activity.
• Study in mice showed that oral adminstration of
flavonoids significantly inhibited the TNF-α
production.
– Biosci Biotechnol Biochem. 2004 Jan;68(1):119-25.

43. Quercetin
43

44. Quercetin
• Belongs to a polyphenolic class of flavonoids.
• Aglycone; basically rutin without the sugar.
• Major bioflavonoid in the human diet.
• Average daily intake 25mg.
• Foods with highest concentrations include
onions, apples, grapes; however, it is ubiquitous.
• Absorption from diet can be up to 20%.
• 64mg in diet can give up to 0.6μM three hours
after ingestion, with the half-life up to 17-25h.

45. Quercetin
• Plasma concentration required to be effective in
cancer is above 10μM. The oral dose to achieve
this may be in the vicinity of 1500mg. With a
relatively long half-life (17-25h), there will be an
accumulative effect over time.
• Anti-inflammatory effects in conditions such as
prostatitis have been shown at 100mg/d.
• In our clinic, we have used doses up to 1000mg
as a single IV and 500mg 3 times a week for
months without side effects except K lowering.

46. Quercetin and Immunity
• Quercetin blocks inflammation, cell migration and
angiogenesis through reduction in iNOS, TNF-α, NFkB,
MMP inactivation, etc.
• Its actions are relevant to all chronic inflammatory
diseases.
• As its anti-inflammatory actions are primary, the question
remains - Where should it be used in acute infections?

47. Quercetin Attenuates NFkB Activation
and Nitric Oxide Production
• Cell culture studies with hepatocytes.
• Cells stimulated with IL-1β.
• IL-1β is a multifunctional cytokine that plays a critical role in
inflammation, immunity, antiviral responses, and a variety of diseases.
• IL-1β stimulates T cells. It is very important in the liver and is implicated
in inflammatory liver diseases.
• IL-1β stimulates iNOS production in hepatocytes during inflammation.
NO binds with SO2 to produce peroxynitrites.
• Peroxynitrites are cytotoxic and capable of injuring invading pathogens
and eliminating altered cells. However indiscriminate destruction of cells
and tissues is implicated in the pathology of liver disease such as
hepatitis.
• Quercetin inhibited the accumulation of nitrite, and decreased the
production of NO.
• Quercetin inhibits the production of NO from LPS stimulated Kupffer
cells.
• In macrophages quercetin and resveratrol decrease LPS stimulated
iNOS.
– J Nutr. 2005 Jun;135(6):1359-65.

48. Quercetin and Cancer
• To date there has been one phase 1 trial of
quercetin IV in cancer.
• Two patients had a positive response with
reductions in tumour markers and tumour size
over the 30-day trial.
• One case was stage IV ovarian, one
hepatocellular cancer.
• In vitro studies show quercetin to be effective in a
wide range of cancers ranging from leukaemias to
lung cancer, melanoma, breast, colon, etc.
• My clinical practice: long-term stabilisation of
lymphoma, breast, myeloma, colon, lung,
mesothelioma and prostate cancers, with both oral
and IV regimes.

49. • Blockade of the epidermal growth factor (EGF)
receptor tyrosine kinase activity by quercetin leads
to growth inhibition in pancreatic tumour cells.
• EGF increased the levels of MMP-2 and MMP-9,
whilst quercetin appeared to decrease these levels.
• MMP-2 and MMP-9 are implicated in the spread of
metastasis.
• EGF stimulation is associated with increased cell
proliferation.
– Anticancer Res. 2002 May-Jun;22(3):1615-27.
Quercetin and Cancer

50. Quercetin in
Myocardial Infarction
• Intravenous quercetin significantly reduces mortality in
myocardial infarction.
– Ukrainian study.
– 57 patients randomised to receive placebo or be
treated with IV quercetin over five days.
– Results:
• reduced size of the heart muscle damage
• reduced size of final infarct
• improved injection fraction
• reduced the risk of subsequent heart failure.
• “This is a safe inhibitor; it is non-toxic, we have very
good long-term survival rate improvement.”
• Results presented at heart failure congress, Milan 2008.

51. Green Tea
51

52. Green Tea
• MMPs and green tea.
• Biochemical research catches up with folk
medicine.
• EGCG from green tea is an effective blocker of
MMP-2 and MMP-9.

53. Green Tea Inhibits Helicobacter
pylori Growth in vitro and in vitro
• Components of green tea have been
shown to:
– be bactericidal
– be bacteriostatic
– inhibit growth of HPE
– prevent the inflammatory effect of HPE on the
gastric mucosa.
– Int J Antimicrob Agents. 2009 May;33(5):473-8.

54. Harpagophytum procumbens
(Devil’s Claw)
• Anti-inflammatory action related to inhibition of
LPS stimulated iNOS, NFkB, COX-2 in
macrophages and mesangial cells.
• Anti-inflammatory action reported as effective
pain control in osteoathritis.
• 50mg of harpagoside gives equivalent analgesia
as synthetic COX inhibitors, but with lower
toxicity.
• Potential use in kidney inflammation.

55. Uncaria tomentosa (Cat’s Claw)
• In vitro studies suggest U. tomentosa inhibits
LPS stimulated TNF-α production 5.5-fold.
• Uses in gastritis and osteoarthritis have been
reported.
• May have a role in Alzheimer’s disease as it has
been shown to bind to beta-amyloid.
• May have some antibacterial activity in both
strept and staph isolates but not fungal nor
pseudomonas.

56. Macrophage Phagocytosis
• Immunomodulatory effects of herbs on
macrophage function.
• Conclusion:
– Standardised extracts of echinacea, cat’s
claw and saw palmetto; main action on
macrophages was in stimulation of
phagocytosis.
– J Med Food. 2007 Mar;10(1):73-9.

57. Obesity and Inflammation
• “These findings provide significant evidence that obesity
is linked to tumour promotion in the pancreas ...
suggests alterations in inflammatory responses and
bioenergetic pathways as the potential underlying
cause.”
– Proc Natl Acad Sci U S A. 2009 Mar 3;106(9):3354-9.
• “Chronic infections, obesity, alcohol, tobacco, radiation,
environmental pollutants, and high-calorie diet have
been recognised as major risk factors for the most
common types of cancer. All these risk factors are linked
to cancer through inflammation.”
– Clin Cancer Res. 2009 Jan 15;15(2):425-30.

58. Common Cold
• Things to consider:
– Influenza or URTI?
– Presentation in otherwise healthy individual.
– Presentation in patient with inflammational
disease already present.
– Secondary infections and complications.

59. 59
Feature Colds Flu
Aetiological agent >100 viral strains; rhinovirus
most common
3 strains of influenza virus:
influenza A, B, and C
Site of infection Upper respiratory tract Entire respiratory system
Symptom onset Gradual: 1-3 days Sudden: within a few hours
Fever, chills Occasional, low grade
(<38.3ÞC)
Characteristic, higher
(>38.3ÞC),
lasting 2-4 days
Headache Frequent, usually mild Characteristic, more severe
General aches, pains Mild, if any Characteristic, often severe
and affecting the entire body
Cough, chest congestion Mild to moderate, with
hacking cough
Common, may become
severe
Sore throat Common, usually mild Sometimes present
Runny, stuffy nose Very common, accompanied
by bouts of sneezing
Sometimes present
Fatigue, weakness Mild, if any Usual, may be severe and
last 2-3 weeks
Extreme exhaustion Never Frequent, usually in early
stages of illness
Season Year round, peaks in winter
months
Most cases between
November and February
(American winter)
Antibiotics helpful? No, unless secondary
bacterial infection develops
No, unless secondary
bacterial infection develops
Adapted from: Roxas M, Jurenka J. Colds and influenza: a review of diagnosis and conventional,
botanical, and n utritional considerations. Altern Med Rev 2007 Mar;12(1):25-48.
Common Cold and Influenza Characteristics

60. 60

61. Advances in Diagnosis and
Management of Influenza
• H5N1 avian flu (H haemagglutinin surface protein, N
neuraminidase surface protein).
• H1N1 swine flu.
• H1N1 virus is not new; the current flu is a new form of
an old virus responsible for the Spanish flu of 1918; re-
emerged in China 1957 and Russia 1977.
• Older people may well have immunity through previous
contact.

62. • Influenza vaccines modified yearly - usually
influenza A H3N2 and H1N1 and one B virus;
only effective in 3 strains in one year.
• There may be up to several hundred strains in
any one year.
• Vaccines for the haemagglutinin and/or
neuraminidase antigen confer up to 70%
protection in the healthy population with those
three viruses considered to be most virulent.
• Less effective in institutionalised elderly patients
- down to 30%.
Flu Vaccines

63. Neuraminidase (NA) Inhibitors
• Influenza viruses attach to cells via sialic acid
receptors.
• NA is needed to remove sialic acids so the
budded virus can detach and disperse.
• Mutations in the sialic binding site can change
the need for NA to increase dispersion.
• Drugs that inhibit NA - oseltamivir (Tamiflu),
zanamir - can be effective in reducing the
duration of the illness. Resistance has been
observed.

64. Echinacea
64

65. Echinacea purpurea
• Echinacea alkylamides suppressed IL-2 secretion by
stimulated lymphocytes.
• This effect was lessened upon oxidation through the
P450 enzymes to carboxylic acids.
• This shows the difference between in vitro effects of
echinacea and potential in vivo effects.
– Planta Med 2006 Dec;72(15):1372-7.

66. Echinacea Induces
Macrophage Activation
• In vivo trial in mice have shown that E. purpurea, when
administered orally, can up-regulate macrophage
function in listeria infections.
• Echinacea stimulates the innate immune system by
stimulating IL-6, TNF, IL-12 and iNOS from
macrophages.
• This resulted in decreased bacterial burden during
infection.
– Immunopharmacol Immunotoxicol. 2008:30(3);553-74.

67. Echinacea purpurea Stimulates
Alveolar Macrophage Function
• Increase in macrophage activity.
• Dose dependent increase in NO and TNF-α on
stimulation with LPS.
• Echinacea stimulates macrophage function in
lung and spleen in rats.
– Int Immunopharmacol. 2002 Feb;2(2-3): 381-7.
• Caution in fibrosis and autoimmune diseases.

68. Echinacea purpurea
• A recent review of PubMed revealed 123 papers on
echinacea and infection.
• Prophylactic treatment with commercially available E.
purpurea did not significantly alter the frequency of upper
respiratory tract symptoms compared with placebo.
– Ann Allergy Asthma Immunol. 2008 Apr;100(4):384-8.
• Extracts from E. purpurea showed consistent and robust
inhibition of HIV - up to 50% inhibition.
– Am J Clin Nutr. 2008 Feb;87(2):488S-92S.
• E. purpurea is considered safe, with no adverse or allergic
reactions in children.
– Can J Physiol Pharmacol. 2007 Nov;85(11):1195-9.

69. Echinacea and the
Common Cold
• A proprietary echinacea extract with a
standardised ratio of alkylamides, cichoric acid
and polysaccharides was found to decrease the
severity and duration of symptoms of the
common cold.
• Mechanisms need to be determined, but
suggested echinacea stimulates the non-
specific immune system.
• Study in 150: 62 got a cold, 26 treated, 31
controls.
• 8 x 5mL dose, then 3 x 5mL for the next six
days.

70. Echinacea for Treatment of the
Common Cold
• Second study on same extract: 282 subjects in
good health: 59 echinacea, 69 placebo.
• Echinacea group severity scores for runny nose,
sore throat, fatigue headache and chills lower by
up to 44%.
• Cough was the same.
• Echinacea group: 50% reduction in symptoms
by Day 4; placebo: same reduction halfway
through Day 5.
– J Clin Pharm Ther. 2004 Feb;29(1):75-83.

71. Echinacea purpurea
• E. purpurea may attenuate the mucosal immune
suppression known to occur with intense exercise, and
reduce the duration of URTI that athletes incur.
• Study involving 32 athletes in high exercise regime
known to affect mucosal immunity such as secretion rate
of mucosal sIgA.
• There was no significant difference in the number of
URTIs but there was significant difference in duration.
– Int J Sports Med. 2007 Sep;28(9):792-7.

72. echinamide
• Developed in Canada by Natural Factors
• German scientist Dr Rudolf Bauer the
worlds most authority on echinacea states
• “Echinamide is unique in that it is has
certain standardized levels of
polysaccharides, cichoric acid and
alkylamides. This new data , which has
produced pharmacolgical results is only
achievable with this product”

73. Quercetin in Acute Infections
• Combine with
–immunostimulatory actions: echinacea,
andrographis, vitamin C
–fish oil
–magnesium.
– Prim Care. 2002 Jun;29(2):231-61.

74. Bromelains
73

75. Bromelains:
Mechanisms of Action
• Introduction of proteolytic activity at inflammatory sites.
• Activation of fibrinolysis activity via the plasminogen-
plasmin system.
• Depletion of kininogen.
• Inhibition of pro-inflammatory prostaglandin biosynthesis
and initiation of PGE1 accumulation (which inhibits the
release of polymorphonuclear leukocyte lysosomal
enzymes).

76. Bromelain and Quercetin
in Sinusitis
• Thins nasal secretions.
• Effective mucolytic agent.
• Inhibits prostaglandins.
• 1987 study showed 85% complete resolution of
sinus inflammation; placebo 40%.
• Doses up to 2000mg/d can be used safely.
• 1000mg/d is more typical.

77. Bromelains and Cytokines
• Proteolytic enzymes have been reported to have
anti-inflammatory effects.
• Bromelain treatment decreased expression of
pro-inflammatory cytokines in ulcerative colitis
and Crohn’s disease.
• Accumulation and activation of inflammatory
cells within the mucosa leads to the tissue
damage that is characteristic of inflammatory
bowel disease.
• Results showed a reduction in Th1 cytokines
with a significant reduction in TNF-α, IFN-
gamma, but not IL-6 nor IL-1β.
– Clin Immunol. 2008 Mar;126(3):345-52.

78. Andrographis
77

79. Andrographis paniculata
• Current evidence suggests A. paniculata alone or in
combination with Acanthopanax senticosus extract may
be more effective than placebo and may be appropriate
alternative treatment for uncomplicated acute URTI.
– J Clin Pharm Ther 2004 Feb;29(1):37-45.

80. Andrographis paniculata
• Double-blind trial using andrographis extract:
– 95 in treatment group, 90 in placebo group.
– Medication taken for 5 days.
– Symptoms included high temperature, headache,
myalgia, sore throat, cough, malaise and eye
symptoms.
• Results: Highly significant improvement in
treated group over placebo.
• Significant symptom improvement was seen in
headache, nasal and throat symptoms together
with general malaise. Temperature was
moderately reduced. Cough and eye symptoms
showed little improvement. The extract was well
tolerated.
– Phytomedicine. 2002 Oct;9(7):589-97.

81. Whey Protein

82. Whey Protein
• Enhances immune function, scavenges free
radicals, and exhibits antimicrobial activity.
• Actions partially due to lactoferrin a peptide
fraction, and its ability to bind excretion-related
iron.
• Lactoferrin is present in exocrine excretions,
nasal discharges, sputum, saliva, etc. Also in
polymorphonuclear neutrophils.
• Actions are also anti-inflammatory and viral
inhibitory.

83. conclusion
• Relationship between immunity and
inflammation.
• Role of abnormal macrophage function in
this
• Beauchamp/ Pasteur
• The use of herbs and natural substances
in modulating these functions