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Y1 Alimentary > Infection and immunology of Gut > Flashcards

Infection and immunology of Gut Flashcards

1
Q

What are the four main mechanisms for protection from infection?

A

Physical Barriers
Chemical Barriers
Bacteria protection
Immunological protection

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2
Q

What are the physical barriers for mucosal defense?

A

Tight epithelial wall
Glycocalyx
Mucous and unstirred layer
Peristalsis to keep things moving along the GI tract

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3
Q

What are chemical barriers for mucosal defense?

A

Bacteriacidal enzymes from paneth cells and acid from stomach

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4
Q

What are bacteria protection for mucosal defense?

A

Commensal bacteria maintain immune system priming and may attack foreign species

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5
Q

What are immunological forms of mucosal defense?

A

Mucosa associated lymphoid tissue (MALT) rich in T cells and B cells whose components can be further categorized into G (Gut) ALT, B (bronchus) ALT etc

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6
Q

What are the two categories of GALT

A

Organised sites of lymphoid tissue such as Peyer’s patches in the small intestine and lymphocytes in mesenteria lymph nodules (where lymph from villi drain)
Disorganised sites inc lymphocytes in the lamina propria (mainly IgA) and lymphocytes in the interstitial space below the basolateral membrane of the epithelium (intra-epithelial cells)

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7
Q

What are Peyers patches?

A

Aggregated lymphoid follicles covered in follicle associated epithelium FAE

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8
Q

Where are Peyers patches found?

A

In small intestine with highest conc in distal ileum

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9
Q

What do Peyer’s patches do?

A

Function as immune sensors since they are capable of monitoring local bacteria and provide protection against pathogenic bacteria

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10
Q

What do Peyer’s patches contain

A

B cells
T cells
macrophages
dendritic cells

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11
Q

What are M cells?

A

Specialised enterocytes in follicle associated epithelium

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12
Q

What do M cells do?

A

Perform transcytosis of luminal bacteria, antigens and proteins.

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13
Q

What do M cells express?

A

IgA receptors that facilitate the transfer of IgA bacteria complex into peyer’s patches

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14
Q

What happens to antigens taken up by M cells?

A

Presented to lymphocytes for assessment and potential immunological response. Activated cells develop gut homing markers and migrate to mesenteric lymph nodes for proliferation

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15
Q

Why is IgA the most abundant antibody in the body even tho IgG is the most abundant circulating immunoglobulin?

A

IgA highly prevalent in mucosal secretions bc MALT associated with IgA plasma cells (B cell secreting a single antibody). The no. of activated plasma cells reflect the bacterial load and up to 90% gut B cells secrete IgA

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16
Q

What is SIgA

A

Secretatory IgA is a dimeric form of IgA

17
Q

Where is SIgA produced?

A

In B cells in lamina propria.`

18
Q

How is SIgA formed?

A

In plasma cell, two IgA bound together by J chain. Dimer binds to special receptor on external basolateral surface of enterocytes (pIgR). Receptor = secretatory component and binds to length of IgA dimer becoming SIgA

19
Q

What does the secretory component of SIgA do?

A

Help IgA move through the enterocyte

Protects the antibody dimer from enzymatic and acidic degeneration

20
Q

What does SIgA do?

A

Binds to pathogens, preventing adherence to mucosal wall.

21
Q

How is antigen specific SIgA production stimulated?

A

Actions of M cells and dendritic cells in Peyer’s patches

22
Q

What happens to mucosal lymphocytes once stimulated by an antigen?

A

Migrate into local mesenteric lymph nodes and drain into lymphatic sstem

23
Q

What is lymphocyte homing

A

Transmigration of lymphocytes into gut mucosa stimulated by tissue specific endothelial adhesion molecules at the site of inflammation

24
Q

What does lymphocyte homing require? - what special type of cells?

A

Specialised post capillary microvascular endothelial cells such as high endothelial venules of lymphoid tissue

25
Q

What is L selectin? - where is it expressed

A

A carbohydrate binding lectin that is constitutively expressed on the surface of lymphocytes

26
Q

What does L selectin do?

A

Mediates the low adhesive interactions that enable leukocytes to roll in post capillary venules and HEVs

27
Q

What happens in HEVs?

A

L selectin mediates lymphocyte rolling by it’s binding to mucosal addressin cell adhesion molecule MAdCAM-1

28
Q

Where is MAdCAM-1 expressed?

A

HEVs of peyer’s patches and mesenteric lymph nodes

Flattened endothelial cells localised in lamina propria of small and large intestines

29
Q

What else does MAdCAM-1 do?

A

Enable lymphocyte recruitment in chronic gut inflammation

30
Q

What are treatment options for irritable bowl syndrome?

A 
Diet modification
Treatment of constipation
Treatment of spasms
Management of stress, anxiety, depression
Most of these target the symptoms^
31
Q

Explain the role of dietary management to treat irritable bowel syndrome

A

Short chain carbohydrates cause symptoms, act as solutes that draw water from GI wall into lumen, causing visceral hypersensitivity (pain) and smooth muscles to spasm and cause diarrhea if water not reabsorbed properly.
These carbs are metabolised by bacterial flora that produce gas that causes even more bloating, spasm or pain

32
Q

Recall the mechanism of coeliac disease

A

Gliadin is not broken down in the stomach, so reaches small intestine and binds to secretory IgA in the mucosal membrane.
Gliadin secretory IgA complex binds to transferrin receptor and are transferred to the lamina propria
Enzyme tissue transglutaminase cuts off amide group from protein
Deamidated gliadin phagocytosed by macrophages and presented by MHC II molecules
leading to activation of immune system - destruction of epithelial cels

33
Q

What is gliadin?

A

33aa peptide component of gluten

34
Q

What is the dietary management of coeliac disease?

A

Gluten free diet (wheat, barley, rye exclusion) and medication. Can also get gluten free foods on prescription.
Factors that affect compliance are lifestyle, eatin out, cross contamination at home and holidays

35
Q

What is Crohn’s disease

A

Causes inflammation anywhere along GI tract - inflammatory bowl disease
Immune related disorder

36
Q

What is an immune related disorder?

A

Immune system triggered by foreign pathogen in GI tract eg mycobacterium paratuberculosis, pseudomonas, and listeria
Inflam response large and uncontrolled and leads to distruction of cells in GI tract

37
Q

Explain the dietary management and nutritional significance of Chron’s disease

A

liquid diet, low fibre/low residue, food reintroduction
Managing strictures: decrease obstruction, pain and gas production. Need to change diet so that food can get through the stricture; fibre can block the intestines. Avoid fibrous parts of fruit and vegetables (skins, seeds, woody stalks), whole- grains, nuts, seeds, gristle and skin from meat and fish, bones etc. May require different consistency e.g. liquidising

38
Q

Explain the dietary management and nutritional significance of Ulcerative colitis

A

Dietary manipulation to minimise exacerbation of diarrhoea.
Diarrhoea: drink fluid, nutritious drinks, replace salt. Eating soluble fibre helps the gut absorb more water from stool. Avoid gas producing foods, high fibre or whole- grain cereals, alcohol (worsens dehydration), caffeine and personal triggers

39
Q

What is ulcerative colitis?

A

An autoimmune disorder where T cells destroy the cells lining the walls of the large intestine

Y1 Alimentary (21 decks)

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