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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
Q

Cause of chronic GI infection

A

Nutrient deficiency and impaired barrier in GI

= more infections

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26
Q

Immune tolerance and Oral tolerance

A

Unresponsive to commercial bacteria and good Ags and self Ags
Unresponsive immune system to previous Ags put in the mouth

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27
Q

Failed oral tolerance

A

Food allergy and Celiac Disease

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28
Q

Negative selection

A

Central Tolerence

T + B cells deleted in the thymus and BM if they react to self Ags

29
Q

Peripheral tolerence is needed for

A

What is found in the lamina Propria in GI and food and commercial bacteria

30
Q

what heppens if you transfer Tregs into another organism

A

They increase oral tolerance

31
Q

Food intolerance

A

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
Q

Food allergy

A

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
Q

How to test type 1 allergy

A

Skin test reaction for the IgE

And serum IgE level

34
Q

How does the IgE dependent Allergy work

1st Exposure

A

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
Q

How does the IgE dependent Allergy work

2nd Exposure

A
  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
Q

Histamine

Mediator of Mast cells

A

SM vasoconstriction - early allergic reaction

Platelet activating factor (PAF)

37
Q

TNF-a and IL-1

Mediator of Mast cells

A

Endothelial cells, inflammation - early allergic reaction

38
Q

Tryptase

Mediator of Mast cells

A

Trypsin-like activity, anaphylaxis - early allergic reaction

39
Q 
Prostaglandin E2 (PGE2) 
Mediator of Mast cells
A

Pain and vascular permeability - late allergic reaction

40
Q

Bradykinin

Mediator of Mast cells

A

Vasodilator and SM contraction - late allergic reaction

41
Q

IL-5

Mediator of Mast cells

A

Sputum eosinophils - late allergic reaction

42
Q

What stimulates mast cells

A

Ag + IL-4, IL-9, IL-13

43
Q 
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)
A
  1. Histamine (PAF)
  2. Th2 cytokines (IL 4,9,13)
  3. Mastocytosis
  4. PAF and Serotonin
44
Q

Treg functions

A

DECREASE : IgE, Th2 cells, mast cells
INCREASE : IgG and IgA

*induced by TGF-B and IL-10

45
Q

Environmental factors that can hep allergy sensitization

A

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
Q

How to Dx: a type 1 allergy

A
  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
Q

no test for type 1 allergy gives you

A

The severity of the allergy

You need Patient HISTORY to make food allergy Dx:

48
Q

IgE mediated allergy example

A

Wheat Allergy (WA)
= alpha -amylase inhibitors, wheat germ agglutinin, peroxidase
Increases prevalence with age

49
Q

What can wheat allergy cause

A

Wheat-dependent exercise induced anaphylaxis (WDEIA)
Occupational Asthma
Rhinitis
Contact urticaria

50
Q

Wheat-dependent exercise induced anaphylaxis (WDEIA)

What are Sx: and Ags

A

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
Q

Wheat-dependent exercise induced anaphylaxis (WDEIA)

Reason it happens

A

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
Q

Non-IgE mediated Food Allergy

A

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
Q

Mixed IgE mediated food Allergy

A

Peanut Allergy - blood testing can confirm IF IGE MEDIATED

54
Q

how does peanut allergy work if non-IGE mediated

A
  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
Q

Reason peanut allergy can cause shock

A

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
Q

Who discovered disease and who said it was from gluten

A

ARETAEUS

Dr. Dicke - said Tx: is no gluten in diet

57
Q

What is Celiac Disease and what are some causes

A

Permanent gluten sensitivity

  1. Failure to thrive,
  2. Delayed puberty,
  3. Autoimmune disorders,
  4. inflammation,
  5. neurological disorders,
  6. Metabolic Disorders
58
Q

CD have a strong association with

A

Autoimmune disease

15%-20% will get an autoimmune disease

59
Q

What makes CD happen

A

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
Q

Sx: of Celiac Disease

How many have it and

A

95% are undiagnosed due to silent presentation
Just don’t complain of any symptoms, diagnosed later in life
1% of US has it

61
Q

How is gluten digested

A

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
Q

What in gluten digestion makes it cause CD

A
  1. The peptides with pro and glutamic acid(-) bind to HLA DQ2.5
    * the HLA DQ2.5 receptor is encoded by DQB102 + DQA105 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
Q

What type of hypersensitivity is CD

A

Type 4

Tissue damage due to self reacting t-cells (CD4 and CD8) = chronic inflammation

64
Q

What makes normal people with no CD digest Gluten

A

They have no HLA DQ2.5 receptor on the T-cells

65
Q

What does gluten cause in its inflammatory response in CD patients

A

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
Q

Which Ab is made against gluten peptide

A

IgA

So no Anit-TG2 Abs can be released

67
Q

IL-15 function

A

Links adaptive and innate immune system by causing T-cells to proliferate

68
Q

SX: that show pt needs to get CD test

A

V,D, ABD pain , constipation

Short stature, dermatitis, delayed puberty, anemia, dental enamel hypoplasia

69
Q

HOW do you test for CD

A
  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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