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GIGU Exam 1 > Gut Immunology - Dr. Shnyra > Flashcards

Gut Immunology - Dr. Shnyra Flashcards

1
Q

Infant Gut Microbacteria and future health is due to

A

Early life exposures (from mom + diet+ environmental)

  • >
    1. Symbiosis : immune tolerance, healthy intestinal meta. + homeo.
    2. Dysbiosis : Immune disease, (asthma, MS), Intestinal disease (IBD), Metabolic Disease (diabetes, obesity)
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2
Q

How if GI microbiota made in the prenatal

A

Established from microflora

Underdeveloped GALT, no Microflora

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3
Q

How if GI microbiota made in the postnatal,

A

After bacteria colonize in neonatal GI, The immune system and microbiota interact and develop the GALT (with Payer’s Patch +ILT) (which regulated the microflora)

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4
Q

ILFs

A

Single B-cell follicles that act as site for IgA production

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5
Q

Where in the GI are we exposed to different Ags

A

GALT

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6
Q

PP and ILF don’t have afferent lymph, how are they exposed to Ags

A

Directly on the epithelial cells from DC

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7
Q

When DC- Ag go into PPs what happens

A

The T-cells are activated and activate B-cells to make IgA plasma cells (in germinal center) that go to lamina Propria to release IgA into Intestinal lumen

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8
Q

Intestinal epithelial cells have PPRs that do what

A

MAMPs recognize the PPRs and this Recruits T-cells and B-cells to help cryptopatches develop into ILFs
= proliferation of epithelial cells and crypts and increase PPs

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9
Q

What do MAMPs do

A 
Recognize PPRs
Release DEFERNES (anti-microbial peptides)
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10
Q

What do goblet cells in the intestinal epithelial cells do

A

Make mucin (proteoglycan gel)

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11
Q

Where are microbiota sensed

A
  1. Enterocytes (SI)
  2. COLONOCYTES (LI)
  3. Paneth Cells (at base of SI crypts)
    Since microbiota by the MAMP = make Antimicrobal peptides (AMP)
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12
Q

Secretory IgA interaction

A

Has a peaceful bacteria-host interaction due to

  • IgA doesn’t activate a compliment system
  • IgA doesn’t activate phagocytes (with Fc)
  • IgA isn’t effected by proteolysis from proteases in stomach, SI, Pancreas
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13
Q

Major AMP in the GI which represents Innate immunity

A

Defensins

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14
Q

How are defensins made
Where is it found
Properties

A

by intestinal epithelial cells (MAMPs)
Inner mucous layer
Clusters of + charge aa and hydrophobic aa side chains = allows defensins to interact to microbial membranes and form PORES in it

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15
Q

What cell is right above the entrance into the Payers Patch

A

The M-cell

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16
Q

Where are most GI bacteria present in the GI

A

Outside layer of mucus over the intestine also epithelial cells
= rapidly killed by macrophages (in Lamina propria) if they penetrate the enterocytes

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17
Q

If DC picks up any penetrating bacteria in GI

A

It brings it to the T-cells and b-cells to make plasma IgA
When T-cells are activates they leave mesentery LN go to the efferent LN into BVs at thoracic duct and then back to mucosa in GI

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18
Q

What causes activation of Treg cells

A
  1. TGF-B = d=upregulate FOXp3 = differentiation of Tregs
  2. Capsular Polysaccharide A(PSA) can promote TLR2 and IL-10 + TGF-B
  3. RA = differentiation of Tregs
  4. IDO = immunosuppressant that causes anergic t-cells = PROLIFERATION of T-regs
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19
Q

Dysbiosis leads to and is a cause of what

A

Dysregulated immune system and inflammation if genetics allows
Changes in diet, environment

Symbiosis= immune regulation homeostasis

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20
Q

What do colonic microbial fermentation make

A

From undigested dietary fibers and carbohydrates ——> SHORT-CHAIN FATTY ACIDS (butyric acid, propionic acid, acetic acid)

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21
Q

Acetate function

A

Increase IL-10 ——> Tregs

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22
Q

Butyrate function

A

Act on DC or directly on Tregs to enhance their function

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23
Q

Malnutrition affects

A

Both GI immune and microflora

Can disrupt the microflora barrier to enteropathogen infection

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24
Q

what causes undernutrition

A

Innate and adaptive immunity

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25
Cause of chronic GI infection
Nutrient deficiency and impaired barrier in GI | = more infections
26
Immune tolerance and Oral tolerance
Unresponsive to commercial bacteria and good Ags and self Ags Unresponsive immune system to previous Ags put in the mouth
27
Failed oral tolerance
Food allergy and Celiac Disease
28
Negative selection
Central Tolerence | T + B cells deleted in the thymus and BM if they react to self Ags
29
Peripheral tolerence is needed for
What is found in the lamina Propria in GI and food and commercial bacteria
30
what heppens if you transfer Tregs into another organism
They increase oral tolerance
31
Food intolerance
Non-immune mediated - missing enzyme needed (lactase) - IBD : can causes chronic cramping, D... - Food poisoning: spoiled food bacteria - stress : thought of food can make you sick
32
Food allergy
Immune mediated (Celiac Disease) - Sensitive to food additives (preservatives like sulfur can cause asthma attack) - Celiac Disease (food allergy to wheat and gluten) - no anaphylaxis TYPE 1 : IgE mediated TYPE 3+4 : non-IgE mediated (use macrophages -> Tcells with Fc receptors)
33
How to test type 1 allergy
Skin test reaction for the IgE | And serum IgE level
34
How does the IgE dependent Allergy work | 1st Exposure
Ag is ingested (peanut, egg....) APC and t-cells see the Ag and activate B-cells B- cells make IgE for the Ag and IgE enters circulation IgE binds to mast cells (FcRe) receptor *only in genetically predisposed individuals
35
How does the IgE dependent Allergy work | 2nd Exposure
1. Ag is ingested and mast cells with the IgEs bind to it 2. Release vasoactive amines (vasodilation) Cytokines (bring WBCs) Lipids 3. Allergen is digested and fragments leave the GI and cause reaction in the skin, respiratory tract, BVs....
36
Histamine | Mediator of Mast cells
SM vasoconstriction - early allergic reaction | Platelet activating factor (PAF)
37
TNF-a and IL-1 | Mediator of Mast cells
Endothelial cells, inflammation - early allergic reaction
38
Tryptase | Mediator of Mast cells
Trypsin-like activity, anaphylaxis - early allergic reaction
39
``` Prostaglandin E2 (PGE2) Mediator of Mast cells ```
Pain and vascular permeability - late allergic reaction
40
Bradykinin | Mediator of Mast cells
Vasodilator and SM contraction - late allergic reaction
41
IL-5 | Mediator of Mast cells
Sputum eosinophils - late allergic reaction
42
What stimulates mast cells
Ag + IL-4, IL-9, IL-13
43
``` When Ag in causing an allergic reaction What causes 1. Distal reactions (urticaria, bronchospasm) 2. GI issues 3. Local symptoms 4. Local acute GI response (diarrhea) ```
1. Histamine (PAF) 2. Th2 cytokines (IL 4,9,13) 3. Mastocytosis 4. PAF and Serotonin
44
Treg functions
DECREASE : IgE, Th2 cells, mast cells INCREASE : IgG and IgA *induced by TGF-B and IL-10
45
Environmental factors that can hep allergy sensitization
VIT D and VIT A and FOLATE = suppress inflammation Gut microflora = suppress allergic response by inducing Tregs and suppressing Basophils and Mast cells High fat = promote inflammation
46
How to Dx: a type 1 allergy
1. Skin prick test = immediate info about IgE sensitization presence (red after 20min-30min) 2. Serum- specific IgE test = blood sent to lab 3. Atopy patch = used for atoptic eczema (how cell-mediated response can be involved with IgE sensitization) 4. Basophil Activation test = in research and developing
47
no test for type 1 allergy gives you
The severity of the allergy | You need Patient HISTORY to make food allergy Dx:
48
IgE mediated allergy example
Wheat Allergy (WA) = alpha -amylase inhibitors, wheat germ agglutinin, peroxidase Increases prevalence with age
49
What can wheat allergy cause
Wheat-dependent exercise induced anaphylaxis (WDEIA) Occupational Asthma Rhinitis Contact urticaria
50
Wheat-dependent exercise induced anaphylaxis (WDEIA) | What are Sx: and Ags
Urticaria and angioedema + upper respiratory obstruction and HTN DURING EXERCISE (When you eat something before exercising). Within 2hrs COMMON Ags: NSAIDS (aspirin), seafood, celery, wheat, cheese
51
Wheat-dependent exercise induced anaphylaxis (WDEIA) | Reason it happens
NORMAL : food is ingested and digested fully = no immuno-reactive allergens enter circulation EXERCISE or ASPRIN: increase absorption of undigested foods(immune-reactive Ags) that go into circulation = Allergic attack
52
Non-IgE mediated Food Allergy
Delayed up to 48hrs Cow’s milk allergy (CMA) - no IgE (no testing for IgE) - can be IgE mediated also (only then will you test for IgE in skin prick test) Usually wrongly labeled as lactose intolerant Tx: if mother is breastfeeding she cant have any Dairy product, no dairy
53
Mixed IgE mediated food Allergy
Peanut Allergy - blood testing can confirm IF IGE MEDIATED
54
how does peanut allergy work if non-IGE mediated
1. Mucosa binds to Ag and makes plasma cells to release IgG for that Ag 2. IgG binds to Ag and activated macrophage 3. Anaphylaxis and mediators from mast cells
55
Reason peanut allergy can cause shock
They can cause production of C3a - macro, baso, and mast ——> PAF + HISTAMINE release by C3aR manner = Vascular permeability and SM contraction = also activated complement of mast cell (Ag does this directly by activating C3a)
56
Who discovered disease and who said it was from gluten
ARETAEUS | Dr. Dicke - said Tx: is no gluten in diet
57
What is Celiac Disease and what are some causes
Permanent gluten sensitivity 1. Failure to thrive, 2. Delayed puberty, 3. Autoimmune disorders, 4. inflammation, 5. neurological disorders, 6. Metabolic Disorders
58
CD have a strong association with
Autoimmune disease | 15%-20% will get an autoimmune disease
59
What makes CD happen
HLA DQ2 and DQ8 make the adaptive immune respond to gluten peptides 1. Make Abs that tag ubiquitous enzyme (TG2) 2. Causes the disease
60
Sx: of Celiac Disease | How many have it and
95% are undiagnosed due to silent presentation Just don’t complain of any symptoms, diagnosed later in life 1% of US has it
61
How is gluten digested
Gluten is 1. PRO-rich (needs Prolyl endopeptidases to be digested in SI) - we don’t have many in SI——> this is normal 2. GLUTAMINE- rich : can be dominated by TG2 ——> - charge glutamic acid ——> this is normal = usually left incompletely digested (like collagen), absorbs only 15-20aa
62
What in gluten digestion makes it cause CD
1. The peptides with pro and glutamic acid(-) bind to HLA DQ2.5 * the HLA DQ2.5 receptor is encoded by DQB1*02 + DQA1*05 for B and a chain = CD have this receptor on t-cells HLA DQ2.5 is + (binds to glutamic acid -) so peptides bind to the T-cells
63
What type of hypersensitivity is CD
Type 4 | Tissue damage due to self reacting t-cells (CD4 and CD8) = chronic inflammation
64
What makes normal people with no CD digest Gluten
They have no HLA DQ2.5 receptor on the T-cells
65
What does gluten cause in its inflammatory response in CD patients
Inflammatory response in the proximal small bowel = mucosa damage and malabsorption 1. CD4 T-cells activation —-> Th1 cytokines TNF-g + IFN-g= MMP 1 +3 from myofibroblasts(matrix degradation and mucosal remodeling/atrophy= malabsorption) 2. CD4 T-cells activation —-> Th2 cytokines IL18,21 IFN-g : make Abs against TG2 and gluten
66
Which Ab is made against gluten peptide
IgA | So no Anit-TG2 Abs can be released
67
IL-15 function
Links adaptive and innate immune system by causing T-cells to proliferate
68
SX: that show pt needs to get CD test
V,D, ABD pain , constipation | Short stature, dermatitis, delayed puberty, anemia, dental enamel hypoplasia
69
HOW do you test for CD
1. Measure IgA to tTG (transglutamase) from blood - tTG-IgA AB test - measure all serum IgA (to make sure pt has no IgA deficiency) 2. Intestinal Biopsy to confirm + identify rare seronegative CD case 3. Genetic Testing : DQ2 and DQ8 present BOTH(last resort to exclude CD)

GIGU Exam 1 (19 decks)

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