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Institute for Functional Medicine exam > Immune > Flashcards

Immune Flashcards

1
Q

What is the role of NF-kB in inflammatory cascades?

A

An inflammatory trigger activates NF-kB, which binds to DNA and leads to activation of iNOS, lipoxygenase (leukotrienes), cyclooxygenase (prostaglandins), TNF, IL1 & IL6, etc; causes oxidative stress

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2
Q

What medications can block inflammatory cascade and where?

A

Biologics block production of TNF, IL-1, IL-6
Leukotriene inhibitors block LOX (e.g., Singulair, Accolate)
NSAIDs block COX
Corticosteroids block NF-kB binding to DNA

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3
Q

What are some botanicals with anti-inflammatory properties?

A

Willow bark, licorice root, boswellia, bromelain, Chinese skullcap, turmeric, ginger, cayenne, aloe vera, green tea

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4
Q

What botanicals have COX modulatory properties?

A

Bromelain, capsaicin, rosemary (carnosol), Chinese skullcap, curcuminoids, feverfew, gingerol, green tea catechins, melatonin (in ginger, seaweed), trans-resveratrol, thymol, willow bark

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5
Q

What botanicals have NFkB modulatory properties?

A

Willow bark, citrus flavonoids (quercetin), Japanese knotweed (t-resveratrol), milk thistle, turmeric, green & black tea, brassica, gingko, garlic, Devils claw, feverfew, boswellia, cats claw, Chinese skullcap, echinacea, pomegranate, ginger, andrographis, thyme, ashwagandha, sulforphane

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6
Q

What enzyme is inhibited by EPA to reduce production of arachidonic acid?

A

Delta-5-desaturase: converts dihomo-GLA to AA

Upregulated by insulin
Inhibited by EPA (from cold water fish, wild game, enriched eggs)

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7
Q

What are food sources of ALA (omega-3 FA)?

A

Flax, walnut, canola, soy, chia, hemp

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8
Q

What are some nutraceutical immunomodulators and how do they work?

A

Vitamin A - supports integrity and function of mucosa; 12,500IU
Vitamin D - stimulates immature immune cells; 4000IU or to serum level of 60-80ng/mL
Glutamine - fuel for cells of the immune system; 5000mg
Probiotics - enhances NK cells activity in the elderly
GSH enhancers NAC, ALA, silymarin - immunomodulation, antioxidant, mucolytic

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9
Q

What are some botanical immunomodulators?

A

Larch arabinogalactan - prebiotic, enhances phagocytosis, NK cells
Ginger - anti-inflammatory
Cat’s claw
Astragalus - bone marrow stimulant, Ig production, activation of NK and T cells
Andrographis - antimicrobial, enhances innate & cellular immunity
Ashwaghanda - adaptogen, reduces hypercortisolism, increases thyroid hormone synthesis, anti-cancer
Echinacea - increased neutrophil chemotaxis, phagocytosis, oxidative burst, NK#s, TNF-alpha
Siberian ginseng - adaptogen, px and tx of colds, reduces severity of HSV outbreaks
Licorice - antiviral, induces interferon, potentiates cortisol
Beta glucans - enhances microbial resistance, mucosal immunity and tolerance to endotoxins, antitumor activity

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10
Q

What are some of the mechanisms through which foods can mediate inflammation?

A

Reducing microbes and LPS translocation
Composition of cell membranes & building blocks of inflammatory mediators
Dampening of inflammatory pathways (eg. eicosanoids) and activation of counter-regulatory pathways
Antioxidant
Through effects on TNFalpha and other cytokines, inducible NO synthase, peroxisome proliferator-activated receptors (PPARs), NF-kB and inflammasome

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11
Q

What are signals for NF-kB?

A

ROS, TNFalpha, IL-1B, LPS, viral infections, ionizing radiation, toxins, antigens, CA-drugs, AGEs, trans fats , heavy metals

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12
Q

What agents/factors can inhibit or modulate NF-kB?

A

Glucocorticoids, calorie restriction, fish oil, gluathione and precursors (ALA, NAC), vitamin C&E

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13
Q

What agents can affect NLRP3 inflammasome activation?

A

EGCG, aloe vera, curcumin, genipin, ginseng, propolis. quercetin, sulforaphone, resveratrol, vitamin c; beta hydroxybutyrate from fasting

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14
Q

What dietary patterns can reduce inflammation?

A

Low glycemic index
High phytonutrients and antioxidants
Inhibition of NF-kB & inflammasome activation and activation of Nrf-2 & PPAR through foods/supplements
Balance of fatty acids
Adequate dietary fiber
Lower salt
Less coffee? (may contribute to rheumatoid factor production)

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15
Q

Whats an indirect way of assessing serum vitamin C levels?

A

Low serum ALP is reflects subclinical vitamin C deficiency

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16
Q

What foods can activate Nrf-2?

A

flavonoids (EGCG, quercetin), polyphenols (curcumin, resveratrol), rosemarinic acid, isothiocyanate, sulforaphane, allicin

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17
Q

What foods can activate PPAR?

A

PPARs are transcription factors; ligand include free FAs, eicosanoids, PGs, LTs, 5-HETE, arachidonic acid metabolites.
Activation ameliorates inflammation and autoimmunity
Omega-3s, ALA, DHA, some omega-6 (LA, AA) and some saturated fats bind to PPAR-alpha

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18
Q

Which enzyme does EPA inhibit to reduce conversion of dihomo-GLA to inflammatory AA?

A

Delta-5-desaturase

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19
Q

What is an optimal ratio of omega-6:3?

A

4-5:1

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20
Q

What are coenzymes required for desaturase metabolism of omega-3 FAs?

A

Zn, Mg, ascorbate, niacin, pyridoxine

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21
Q

What factors impact oxidative effects of red meat?

A

Greater oxidation w/larger interprandial periods
High heat, microwaving and cooking with seed oils cause high oxidation
Lower fat red meat is associated with more oxidation
Meat frozen x 6 months have less oxidation than meat chilled for 20 days

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22
Q

What is the problem with nightshades?

A

Alkaloids in nightshades may increase intestinal permeability

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23
Q

What are long-term consequences of keto diet?

A

Increased risk of NAFLD, insulin resistance, shifts in microbiome (increased Desulfovibrio, Enterobacteria, Bacteriodetes, Akkermansia; decreased Bifidobacter, Firmicutes)

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24
Q

What is a foundational program to lower inflammation?

A

Diet: Low glycemic load, high fiber and phytonutrient content, 4-5:1 omega-6/3 ratio, low/no trans-fats
Adequate intake of zinc, magnesium, ascorbate, niacin & pyridoxine to optimize desaturase metabolism of PUFAs

Supplements: broad spectrum multiple to cover bases for enzyme production, omega-3s, anti-inflammatory phytochemicals/botanicals

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25
Q

What is the acute-phase response and how is it mediated?

A

Systemic response to local trauma (DAMPs) and pathogens (PAMPs).
Mediated by cytokines released by macrophages & monocytes (IL-6, IL-1B, IL-8, TNF-a, INF-g)

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26
Q

What are the systemic responses to acute inflammation?

A 
Hepatic synthesis of plasma proteins (CRP, fibrinogen, serum amyloid protein, haptoglobin, ceruloplasmin, alpha1-acid glycoprotein)
Leukocytosis
Thrombocytosis
Increased body temp (IL-6)
NF-kB activation and translocation
Shift from anabolic to catabolic
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27
Q

Which markers increase with acute inflammation (rapid and slow)? Which markers decrease?

A

Rapid increase in: CRP, serum amyloid A, glutathione (1-2 days)
Slow increase: coagulation proteins, complement, transport proteins (severals days-week)

Transient Decreases: serum albumin, transferrin, retinol-binding protein, antithrombin, AFP, IGF-1, TBG (diverted to increased proteins)
Decreases in plasma iron and zinc

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28
Q

What is leukopenia and its potential causes?

A

WBC <4,300 cells/mm3
Most common cause is infections; also folate, B12, or Cu deficiency

Drug-induced neutropenia: Abx, CBZ, valproate, anti-thyroid, anti-depressants, clozapine, anti-inflammatories, CV meds, CA Rx, toxins, heavy metals (Hg, As, Au)

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29
Q

What is leukocytosis and its potential causes?

A

WBC >11K
Acute phase reactant - increases due to infection, inflammation, allergy, malignancy, obesity, stress, demargination (steroids, lithium, beta-agonists)
Note - mild increase in WBC increases CV risk

Neutrophilia - acute bacteria; also smoking, obesity
Lymphocytosis - acute viral
Monocytosis - chronic infection, inflammation
Eosinophiia - allergic, parastitic

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30
Q

What are indications for ESR?

A

Distinguish inflammatory vs allergic
Chronic or persistent infections (osteomyelitis, pelvic inflammatory disease, TB)
>100mm/hr: SLE, PMR, RA, IBD, CKD, others
T1/2 = days to weeks

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31
Q

What is CRP and what are some indications for testing it?

A

Produced in smooth muscle and liver in response to IL-6
Activates complement, binds LDL
Increased with BMI, smoking
T1/2 = 4-19hours

Indications: IBD, CAD, DM, periodontal disease, obesity, arthritis, SLE, thyroid disease
Note: hsCRP is used as a cardiac risk marker, vs CRP for chronic inflammatory disorders

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32
Q

What is fibrinogen?

A

Acute phase reactant which increases blood viscosity
Increases typically occur several days after injury/infection (t1/2=3-4 days)
Increases with ASHD, smoking, inactivity, excessive alcohol, estrogen therapy; Baseline level predicts risk of MI/CVA

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33
Q

What are effects of complement activation?

A

Enhances phagocytosis, clumping of antigens, chemotaxis, cell lysis and plasma protein exudation.

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34
Q

What is the significant of decreased complement? Which proteins?

A

Low C3, C4, CH50 - indirect evidence of extensive consumption due to immune-complex mediated inflammation (ie in SLE, vasculitis) or hereditary angioedema (where lack of C1 esterase inhibitor allowed unopposed lysis of C2 & C4, so C4 levels low)

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35
Q

What is the significance of increased complement split products (C3a, C4a, C5a)?

What are indications?

A

These are anaphylatoxins causing bronchospasm, mast cell degranulation, vascular permeability, chemotaxis and cytotoxic ROS.
C3a increased w/ acute Lyme, active SLE, vasculitis, asthma, pancreatitis, pregnancy
C4a increased w/chronic Lyme, CFS, DM, MS, HIV, mycotoxin exposure (?)

Order if: suspected immune activation if other markers negative, suspected mast cell activation, MS, suspected invasive fungal infection, Lyme disease, autoimmune

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36
Q

What are Th1 dominant diseases? (IFN, TNF, IL-1, IL-2, IL-12)

A

RA, MS, thyroiditis, Lyme arthritis, Crohns, Type 1 DM

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37
Q

What are Th2 dominant diseases? (IL-4, IL-5, IL-6, IL-10, IL-13; B-cell mediated activation of histamine release; increased IgE, IgG4)

A 
Allergic diseases, asthma, contact dermatitis
Scleroderma
UC
SLE
Pregnancy
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38
Q

What is IL-17? What is its significance in MS therapy?

A

Produced by Th17 cells
Mediates mucosal immunity and is primary driver of chronic inflammation (via NFkB stimulation)

Note: in IL-17 induced MS, IFN-B may be pro-inflammatory; predicts efficacy of this drug in MS

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39
Q

When should cytokine testing be done?

A

Screening for suspected inflammatory disorders, especially when other markers are negative;
Profile & pattern better than individual cytokines
(ie Th1/Th2/Th17)

Up-regulation of cytokines predates onset of RA

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40
Q

What are natural killer cells?

A

Large, granular cytotoxic lymphocytes; part of innate immunity and activated by cytokines, antibodies, acute stress, target cell ligands

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41
Q

What decreases activity of NKCs?

A

Aging, cancer, cancer Rx, chronic or recurrent infections (HIV, herpes, influenza, hep C), CFS/CFIDS, inflammation, autoimmunity, obesity, smoking, chronic stress, depression, EPA

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42
Q

What are indications for NK testing?

A

Rx monitoring (chemo, autoimmune), recurrent viral infections, autoimmune thyroiditis, chronic fatigue, cancer;

Suspected increased in activity: Increase in NK activity is associated with exacerbation of autoimmune thyroid disease, recurrent unexplained miscarriages

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43
Q

What is ANA and when would you test it?

A

Non-specific autoantibodies vs various components of the cell nucleus; increases imply a break in immune tolerance

Suspected SLE, Sjogrens, scleroderma, mixed connective tissue disease, dermatomyositis, polyarteritis nodosum, MS, thyroiditis, certain malignancies, infections

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44
Q

What is anti-citrullinated protein Ab?

A

Citrulline converted from arginine (due to inflammation), creating an antigenic molecule.
98% specific for RA; predictive of onset

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45
Q

What are the half-lives of IgG, IgE and IgA? What are their functions?

A

IgG - 23 days; protects tissues, activates complement
IgE - 2-3 days; attaches to mast cells and causes histamine release, anti parasitic
IgA - 5-6 days; protects mucosa (luminal, secretory IgA), clears absorbed food and pathogens which have breached mucosa (serum IgA)

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46
Q

How are IgE allergies evaluated?

A

Skin prick - high sensitivity, low specificity; variable with different antigen sources and preparation
- false positives
Food challenge - gold standard

47
Q

What are ATMs associated with food allergies?

A

Antecedents: genetics, delayed exposure to allergens, lack of biodiversity, C-section, bottle feeding, prenatal (and transgenerational) smoke exposure

Triggers: medicines, toxins, inadequate vitamin D/omega-3/antioxidants, inflammatory foods

Mediators: barrier permeability, hypochlorhydria, stress obesity, dysbiosis

48
Q

What are therapeutic options for food allergy?

A

Avoidance
Allergy shots, SL or oral immunotherapy
Vitamin D, vitamin A, zinc, EFA
Probiotics

49
Q

What is a common presentation of IgE food/inhalant cross-reactions?

A

Oral allergy syndrome
(generally heat and digestion labile)
60% of IgE Food reactions are cross reactions with inhalant IgE allergens (usually the sensitizing agent)

50
Q

What are limitations to IgG Testing?

A 
Analytical limitations (split sample non-coherence)
Inter-lab variation 
Immunoglobulin subclass deficience
Interference from steroids
51
Q

What are alternative methods of testing for food reactions?

A

IgA testing
MRT testing (mediator release test) - measures subtle volumetric changes in WBCs
ALCAT testing (antigen leukocyte antibody test) - tests delayed sensitivity reactions, similar to MRT
MRT & ALCAT - no peer-reviewed research

52
Q

What causes histamine intolerance?

A

Eating too much histamine or biogenic amine-containing foods
Reduced DAO/DAO activity
(DAO inhibited by alcohol, drugs, enterocyte damage)
Increased histamine due to allergy, microbes eating histidine, in leftovers

53
Q

How to assess and treat histamine intolerance?

A

Labs: serum or whole blood histamine, serum DAO <10U/mL

Treatment: Low histamine elimination and challenge,
DAO enzymes w/meals
identify & treat cause
Vitamin C & B6 may help support DAO fxn
5Rs (gut inflammation & damage, SIBO) or 6R allergy protocol

54
Q

What is mast cell activation syndrome and how does it differ from histamine intolerance?

A

Condition with symptoms associated with overproduction of mast cell mediators affecting 2 or more organs.
Histamine is one of these mediators, so intolerance can occur with MCAS.

55
Q

What are symptoms of histamine intolerance and MCAS?

A

HA, urticaria, hypotension, facial flushing, D/N/V, vertigo, abdo pain, congestion, rhinorrhea, asthma

56
Q

What foods are high in histamine?

A

Fermented foods, aged cheese, wine, processed meats, older foods, citrus

57
Q

What are symptoms of tyramine sensitivity?

A

Headaches, hypertension, allergy-like symptoms.

tyramine in aged, spoiled, fermented foods

58
Q

What are options for treating high oxalate?

A 
Hydration
Increase citrate (foods and supplements)
Reduce high oxalate foods
Probiotics
B6 to support conversion of glyoxalate to glycine
Reduce dysbiosis and fungi
59
Q

What is the mechanism of salicylate intolerance?

A

Inhibits COX, increases LOX

Increases pro-inflammatory cysteinyl leukotrienes (5-HPETE) and skews towards Th2

60
Q

What are symptoms of salicylate intolerance?

A

Asthma, GI upset, tinnitus, urticaria, headaches, rhino sinusitis, nasal and sinus polyps

61
Q

What foods contain salicylates?

A

Apples, avocadoes, berries, cherries, grapes, peaches, plums, fermented foods, alcohol

62
Q

What genetic SNPs are associated with celiac disease?

A

HLA-DQ2 (95%), HLA-DQ8

63
Q

What markers are used to diagnose celiac disease?

A 
Total IgA
IgA Anti-tissue transglutaminase
IgA Anti endomysial antibody
Deamidated gliadin IgG and IgA
Ig A and IgG anti-gliadin to expand beyond celiac (ie non-celiac gluten sensitivity)
64
Q

What is optimal EPA & DHA intake?

How much GLA should be taken with EPA/DHA and why?

A

Aim for 3-6g/day EPA/DHA (<1.5g/day not likely to be effective for inflammation, no benefit >7g) 1.5:1 EPA/DHA
GLA 3g; take w/EPA to inhibit conversion to arachidonic acid
EPA/DHA ratio 1.5/1
Note Total omega Rx: concurrent GLA, ALA, DHA, EPA – stimulates resolvins

For vegetarians: 5-10% of ALA convert to EPA (chia seeds more efficient than flax; DHA from algal oil, with some retroconversion to EPA)

65
Q

What is the DHA recommendation for people with ApoE4 and Alzheimer’s risk?

A

Early supplementation of DHA in ApoE4 may decrease risk of AD, but must be started before symptoms start and large doses of omega-3 (>1g) are needed for brain bioavailablity

66
Q

What are the omega-3 index risk zones for CVD?

A

<4% - highest risk
4-8 - moderate risk
>8 - low risk

(in % of erythrocyte FAs)

67
Q

What are ways to reduce omega-6:3 ratio?

A

Increase omega-3 w/EPA& DHA
Desaturase competition w/EPA or ALA
Modulate desaturase activity - lower glucose & insulin, avoid or reduce alcohol & glucocorticoids
*recommend concurrent GLA to reduce AA conversion to pro-inflammatory mediators

68
Q

Is there a risk of A fib w/omega 3 supplementation?

A

Possibly - U-shaped relationship
Lowest and highest % RBC DHA had highest risk
Aim for omega-6 index 9.2-10.4%

69
Q

What is the preferred method of measuring omega-6/3 index?

A

RBC or blood spot

70
Q

What are the multiple anti-inflammatory mechanisms of turmeric?

A

Decreases: NFkB, COX, LOX, iNOS, matrix metalloproteinases, cytokines (TNFa, IL 1,2,6,8,12, chemokine); Increases Nrf2 (regulates antioxidant proteins)

Use for inflammatory conditions, autoimmunity

71
Q

What are the anti-inflammatory mechanisms of ginger? What are the most common side effects and warnings?

A

Decreases NFkB, COX (PG-E2), LOX (LTB4), ROS-generating enzymes; Activates PPAR

Most frequent s/e is GI upset; may inhibit platelet aggregation

Use for inflammatory conditions

72
Q

What are the anti-inflammatory mechanisms for Boswellia? What is it used for?

A

Inhibits 5-lipoxygenase (LT, PgE synthesis), NFkB

Use for asthma, OA, IBD, RA

73
Q

What are the anti-inflammatory mechanisms for bromelain?

A

Proteolytic enzymes w/anti-inflammatory and analgesic properties

Inhibits thromboxane & prostaglandin synthesis, bradykinin, COX2
Increases fibrinolytic activity

Use for trauma, post-surgical, sinusitis, OA
(take on empty stomach)

74
Q

What are the anti-inflammatory mechanisms for Devils claw?

A

Inhibits NFkB, LOX, COX-2, iNOS
Use for DJD/OA, low back pain

few side effects, limited to GI upset

75
Q

What are the anti-inflammatory mechanisms for quercetin?

A

A flavonol flavonoid found in apples, berries, brassica, onions, tea, tomatoes, elderberry, dried oregano
Inhibits phospholipase A2, COX, LOX; inhibits histamine release from mast cells and basophils;
Pro-apoptotic

Use for allergies, asthma, atopy

76
Q

What are the anti-inflammatory mechanisms for capsicum?

A

Topical relief of pain due to depletion of substance P in sensory fibers
Inhibits COX2 and iNOS

Use for low back pain, diabetic neuropathy

77
Q

What are the anti-inflammatory mechanisms for green tea?

A

Green tea contains EGCG and other flavonols
Inhibits IL-8 production in airway, CD-4 T cell production in MS, LOX
Inhibits NFkB and decreases IL-6, IL-8 and TNFa

Use for: CA and most inflammatory conditions
Note: increase EGCG BA w/quercetin and fish oil; extract from green tea by steeping for 3-5 minutes

78
Q

What are the anti-inflammatory and analgesic mechanisms for CBD?

A

CB1 (brain, nerves) and CB2 (periphery, immune system) receptors found on immune cells
Anti-inflammatory: Induce apoptosis, inhibit cell proliferation, suppression of cytokines and induction of Treg cells;
Analgesic: endocannabinoid receptor activity, reduce inflammation, interact w/neurotransmitters

79
Q

What is the allergy 6-R program?

A

Reduce symptoms
Remove (important to consider cross-reactions)
Replace (hypochlorhydria important consideration)
Reinoculate
Repair
Rebalance

80
Q

What interventions can be done for dust mite allergies?

A 
Symptom diary to identify where,
SLIT 
saline nasal spray or neti pot daily
Dust mite covers on bedding
HEPA filter in bedroom
Remove bedroom carpet, upholstered furniture
Keep windows open
Wash bedding in hot water
HEP vacuum or mop floors weekly, dust w/damp cloth
81
Q

What is filaggrin and its significance in atopy?

How can this be mitigated?

A

Epidermal barrier protein which forms NMF (natural moisturizing factor).
Fillaggrin mutation is associated with atopic march (allergic rhinitis, asthma, allergic sensitization) and more common in Northern European ancestry (possibly due to vitamin D deficiency?). May increase topical chemical uptake.

Dilute bleach soak (anti-inflammatory, inhibits NKfB), apply ceramide (most abundant fatty acid in the stratum corneum), ceramide + probiotic

82
Q

What are strategies for reducing allergy symptoms? (part of 6R approach)

A

Antihistamines: bromelain, quercetin, vitamin C, stinging nettles, butterbur, luteolin, palmitoylethanolaminde PEA
Nasal irrigation (saline, could add some berberine, garlic)
Boswellia (5LOX inhibitor)
Magnesium (vasodilation)
Antipruritics - topical ceramide, homeopathic sulfur 30c-200c PRN
Bicarb 1/4-1/2 tsp in water QID prn (to prevent hives, EOE, angioedema, exercise-induced)

83
Q

What inflammatory mediators are released from mast cells?

A

Histamine, serotonin, PG-D2, proteases (tryptase), SOD, peroxidase, LTs, heparin, platelet activating factor, chemokines

84
Q

What conditions are strongly associated with mast cells?

A

Interstitial cystitis, asthma, atopic dermatitis, psoriasis

85
Q

What are molecular triggers for innate immunity?

A 
Microbes
Foods (gliadin, AGEs, lectins, beta-glucans)
Trauma, ischemia
Toxins, free radicals
cellular debris (DAMPs)
86
Q

What are examples/sources of DAMPs?

A

Debris from injured or necrotic cells (DNA or mitochondrial bits, purines (ATP, adenosine, uric acid), heat shock proteins
Endogenous, non-infectious molecules
AGEs, misfolded proteins

87
Q

What is the role of toll-like receptors?

A

Activate maturation and differentiation of dendritic cells, which in turn induce T cell maturation (into Th1, Th2, Th17 or Tregs)

88
Q

What nutraceuticals, Rx, etc suppress IL-17 cytokines?

A

Vitamin D, retinoid acid, zinc, statins, flavonoids, licorice root, triptolide

89
Q

What are inflammasomes?

A

Cytosolic intracellular receptors activated by intracellular PAMPs and DAMPs; leads to assembly of large multi protein complex which activates IL-1B and IL-18 (highly inflammatory)

90
Q

What are some causes of chronic NFkB up regulation?

A

Chronic infection, cancer, autoimmune disease, depression, aging, chronic neurodegeneration

91
Q

What are inflammatory triggers for adaptive immune response?

A

Allergens, lectins (proteins, glycolipids, synthetic chemicals), pathogens, cellular debris

92
Q

What are mechanisms of microbial triggers to autoimmunity?

A

Molecular mimecry, epitope spreading, bystander activation (“waking up” dormant immune cells), immortalization of infected B cells, super-antigens, immune complex (ie antibodies + antigen) deposition into tissues

93
Q

How can long-term chronic infections affect individual immune response?

A

The infectious disease conundrum: viral and bacterial phenotypic resistance, pathogen influences on host immunity, Th1 vs Th2 host immune response, genetic variation and susceptibility, cascade of chronic dormant infection activations

Eg. viruses implicated in autoimmunity: CMV, EBV, Coxsackie B, influenza A, herpes, MMR
- latent infection of memory B cells by EBV - a Trojan horse which smuggles virus into the CNS

94
Q

Aside from Borrelia, what other co-infections are related to ticks?

A

Babesiosis, bartonella, rickettsia, human granulocytic anaplasmosis, human monocytic ehrlichiosis;
Imitators: Powassan virus, West Nile, Chlamydophila pneumonia, CMV, EBV, parvo, HSV, Strep A (PANDAS), Alpha-gal

95
Q

What are the 4 basic strategies for stealth pathology?

A

Immunosuppression
Genetic, phase and antigenic variation
Physical seclusion
Secreted factors

96
Q

How does Lyme disease follow the 4 basic strategies for stealth pathology?

A

Immunosuppression: analgesic, anticoagulant and immunosuppressive factors released by tick saliva and Borrelia

Genetic, phase and antigenic variation: Borrelia burgdorferi engages in gene switching, mutation & recombination, variable antigen expression, auto-induction of dormant organisms (dormant cyst state; evades abx), fibronectin binding

Physical seclusion: intracellular “cloaking” by binding to proteoglycan, collagen, plasminogen, integrin & fibronectin, making it invisible to immune system

Secreted factors: pheromones to auto-resuscitate, adhesion and porin proteins allow B. burgdoreri to adhere to cells and pierce cell membrane to gain entry

97
Q

What are some strategies for modifying biofilms?

A

Lactoferrin, colostrum, serum-derived immunoglobulins, probiotics & probiotics, enzymes, xylitol, EDTA, Stevia

98
Q

What is the 2-tier system for Lyme testing and what is its limitation?

A

1) Screen with ELISA or immunofluorescence
2) Confirmation w/Western blot
Note: 2-tier test becomes positive between 4-6 weeks

High specificity (99-100%), but poor sensitivity (50-75%); avoids false-positives, but limits its use in diagnosis
- 1/2 of patients get false-negative
Therefore, ideally use combination of tests including direct PCR
99
Q

What are symptoms of Lyme disease?

A

Fatigue, night sweats, low-grade fever, sore throat, swollen glands, stiff neck, migrating arthralgias, migrating myalgia, sleep disturbance, poor concentration, memory loss, irritability, anxiety, tinnitus, cranial nerve disturbance, HA, dizziness; progressive over time w/chronic lyme

100
Q

What is CD57’s significance in Lyme disease?

A

Chronic Lyme suppresses CD-57 subset of NK cells.

Abnormally low CD-57 can be used as marker of how active the infection is

101
Q

How can Lyme be distinguished from autoimmunity based on C3a and C4a levels?

A

Increased levels of C3a - active autoimmunity

Increased levels of C4a - chronic Lyme; greater in MSK vs neuro Lyme

102
Q

What are the functions of the gut microbiome?

A

Nutrient harvest, energy metabolism
Breakdown of plant polysaccharides
SCFA production
Amine/amino acid production - neurotransmitters
Production of estrogenic compounds (enterodiol, enterolactone) from lignans
Vitamin Synthesis (B12, biotin, K)
Modulates bone density
Toxin metabolism
Epithelial health - healing, mucus, barrier integrity, HSP 25/72
Immunoregulation - increases IL-10, TGFB, sIgA, apoptosis of Th1 cells; decreases NFkB, TNF, IL-12
Inhibits pathogenic bacteria - decreased pH, bacterial binding and invasion of epithelium, increased B-defensins

103
Q

What factors can lead to dysbiosis?

A

Host genetics (mutations in NOD2, IL23R, ATG16L, IGRM)
Age
Diet (low fiber, high fat, high simple carbs), stress/fear/anger
Hospital birth, altered birth exposure to microbes
Antibiotics, medications, alcohol, hygiene
Chronic maldigestion
Chronic constipation

104
Q

How does psychoemotional stress impact the microbiome?

A

Stress suppresses Lactobacillus, Bifidobacter and sIgA
Catecholamines stimulate gram-neg Yersenia, Pseudomonas
Anger or fear increase B fragilis

105
Q

What are consequences of dysbiosis?

A

Immunosuppression
Immune activation
Inflammation
Intestinal permeability

106
Q

Which commensal bacteria are associated with protection against inflammatory/autoimmune disease?

A

Bifidobacterium
Bacteroides
Clostridium
Lactobacillus

107
Q

What tests can be used to assess gut dysbiosis?

A

Stool testing - microscopy, PCR, metabolites, 16s rRNA sequencing, ova & parasite, enzyme immunoassay (Giardia, Cryptosporidium, E. histolytica, trichomonas)
Breath testing
Urinary OAT

108
Q

What are mechanisms for effects of S boulardii?

A 
Trophic effects on brush border enzymes
closure of gut permeability
anti-inflammatory
immunostimulatory
Inhibition of Toxins
Resistance to bacterial overgrowth
109
Q

What is Dr. Sult’s protocol for chronic Lyme (from case study)?

A

Stevia 15drops BID (6wks on, 2wks off)
Biocidin LSF 2 pumps BID (6wks on, 2wks off)
Colloidal silver 20ppm 1oz/daily (6wks on, 2 wks off)
Colostrum for biofilm inhibition

6wks is course of therapy, 2 wks wash out allows renewal of growth and loss of some of the stealth pathology, then treat again

Plus treat all other matrix imbalances; start in the gut

110
Q

What is the sensitivity and specificity of ANA & its subtypes?

A

ANA: 93% sensitive for SLE, 57% specific
- 85% sensitive for Sjogrens, scleroderma

Anti-dsDNA - 97% specific for SLE
Anti-SSN/la - 94% specific for Sjogrens

111
Q

What are symptoms of severe nickel allergy syndrome? What are foods which contain nickel?

A

Skin & GI symptoms, allergic contact mucositis

Foods: whole grains, cocoa, tea, gelatin, baking powder, soy, legumes

112
Q

What are symptoms associated with MSG?

A

Headache, asthma, flushing, facial pressure or tightening, numbness, palpitations, nausea, urticaria, rhinitis

113
Q

What are the risks of carrageenan?

A

Degradation of carrageenan by food processing, gastric acid, and bacteria may form toxic & inflammatory poligeenan

Institute for Functional Medicine exam (7 decks)

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