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immunology of the gut Flashcards

1
Q

What is SA of GI tract and what does that mean for its immunology?

A

SA 200m2 so exposed to massive antigen load (resident microbiota, dietary antigens, pathogens

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2
Q

What is the gut in a state of immunologically?

A

In a state of restrained activation to balance tolerance and active immune response.

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3
Q

What does immune homeostasis of the gut require?

A

Presence of bacterial microbiota

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4
Q

What is microbiota? What is microbiome?

A
  • Microbiota is mixture of microorganisms making up a community in a specific anatomical compartment.
  • Microbiome are collective genomes of all the microbiota of all anatomical niches in the body
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5
Q

What is gnotobiology?

A

Selectively colonises germ free animals and compares with controls to see effects of different microbiota

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6
Q

How many gut bacteria in the body? What are the major phyla? What do they provide for us?

A
  • 10^14 gut bacteria.
  • 4 major phyla: bacteriodetes, firmicutes, actinobacteria, proteobacteria + viruses/fungi.
  • They provide traits we haven’t evolved on our own (essential nutrients, metabolise indigestible compounds, defense against colonisation by opportunistic pathogens, intestinal architecture)
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7
Q

What host factors stimulate gut bacteria? What host factors decrease bacteria numbers?

A
  • Ingested nutrients & secreted nutrients encourage bacterial growth (increase cell numbers).
  • Chemical digestive factors, peristalsis, contraction, defacation lead to bacterial lysis and elimination (decreasing cell numbers)
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8
Q

How do the bacterial numbers vary in different parts of GI system and why?

A
  • In stomach lower numbers because HCL, pepsinogen, gastric lipase keep numbers low.
  • In duodenum, liver bile acids keep numbers low.
  • In pancreas, trypsin, amylase, keep them high.
  • In illeum higher.
  • In colon no digestive factors keeping them down (10^12)
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9
Q

What are symbionts? Commensals? Pathobionts?

A
  • Symbionts live with host but no benefit or harm to each other.
  • Commensals benefit from association but have no effect on host.
  • Pathobionts are symbionts that don’t normally cause inflammatory response but can cause inflammation/disease when they start replicating
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10
Q

What are causes of dysbiosis? What does dysbiosis then cause?

A
  • dysbiosis: instability of the gut microbiome
  • Infection, inflammation, diet, xenobiotics, hygiene, genetics.
  • Dysbiosis causes pathogens producing bacterial metabolites/toxins affecting body
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11
Q

What are examples of toxins produced from dysbiosis and their associations?

A
  • TMAO (increases cholesterol deposition in arteries - atherosclerosis)
  • 4-EPS (associated with autism)
  • SFCAs (decreased in IBD, increases in stress/neuropsychiatric disorders),
  • AHR ligands (associated with MS, RA, asthma)
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12
Q

What is the mucosal defence from infection?

A
  • Physical barriers –> anatomical (epithelial barriers, peristalsis).
  • Chemical barriers - enzymes, acidic pH.
  • Epithelial barrier: mucus layer made of goblet cells, epithelial layer with tight junctions.
  • In small intestine paneth cells in crypts of lieberkun secrete antimicrobial peptides (defensins) & lysozyme.
  • Commensal bacterial occupy ecological niche
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13
Q

What is immunological defence following infection?

A

MALT (mucosa associated lymphoid tissue) & GALT (gut associated lymphoid tissue)

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14
Q

What is MALT, where is it found? What is its structure? Which area is rich in immunological tissue?

A

MALT - mucosa associated lymphoid tissue, found in submucosa below epithelium as lymphoid mass containing lymphoid follicles. Surrounded by HEV post-capillary venules allowing easy passage of lymphocytes. Oral cavity rich in this tissue (eg tonsils)

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15
Q

What is GALT? What does it contain?

A
  • Gut-associated lymphoid tissue.
  • Both adaptive & innate immune response.
  • Has B & T cells, macrophages, APCs and specific epithelial & intra-epithelial lymphocytes.
  • Non-organised - intra-epithelial lymphocytes (eg. T cells, NK cells, lamina propria lymphocytes).
  • Organised: peyer’s patches, caecal patches, isolated lymphoid follicles, mesenteric lymphoid nodes
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16
Q

What is non-organised GALT?

A
  • Everything comes from stem cells in crypts, migrate to top of microvillus.
  • Central part of villus made of lamina propria and T, macrophages, DC found here.
  • Intra-epithelial lymphocytes will be dotted between enterocytes
17
Q

What are peyer’s patches? Where are they found? Structure? What do T & B cells require? How is antigen taken up?

A
  • Immune sensors found in submucosa of small intestine (mainly distal ileum).
  • Aggregated lymphoid follicles covered with follicle associated epithelium FAE which has no goblet cells, no secretory IgA and no microvilli.
  • Has dome area with DC, naïve t cells (intrafollicular) and B cells.
  • T & B cell development requires exposure to bacterial microbiota.
  • Antigen taken up by M (microfold) cells within FAE that express IgA receptors so facilitate transfer of IgA bacteria complex into peyer’s patches
18
Q

What can trans-epithelial dendritic cells do?

A

They can open up tight junction proteins and directly sample bacteria outside and go back to activate lymph nodes

19
Q

How is the B cell adaptive response made in the gut?

A
  • M cells take up pathogen. Excreted into pocket in inner surface of enterocyte containing APCs which engulf pathogens & present them with MCH-II molecules on surface.
  • DCs migrate to peyer’s patch where T, B, DC cells aggregate and form organised lymphoid tissue.
  • mature naive B cells express IgM in peyers, but on antigen presentation class switches to IgA)
  • B cells activated and mature to become IgA secreting plasma cells that populate lamina propria.
  • T & epithelial cells influence B cell maturation.
  • Most of B cells secrete IgA that binds luminal antigen - preventing adhesion & invasion
20
Q

What is lymphocyte homing? Where do lymphocyte go after the peyer’s patches?

A
  • From peyer’s patches lymphocytes travel to mesenteric lymph nodes & return to circulation via thoracic duct.
  • From there either enter peripheral immune system (skin, tonsils, BALT) or return to intestinal mucosa via vessels in lamina propria.
21
Q

Why rapid turnover of enterocytes and goblet cells?

A
  • Short life span 36h because enterocytes first line of defense against GI pathogens and may be affected by toxic substances in diet.
  • Any lesions will be short lived.
22
Q

How does cholera cause infection and what does it cause?

A
  • Caused by vibrio cholerae serogroups 01 & 0139.
  • bacteria reaches si, makes contact with epithelium & releases cholera enterotoxin.
  • Internalised by retrograde endocytosis.
  • High levels of cAMP cause active secretion of salts and water causing profuse watery diarrhoea. (CFTR-channel)
23
Q

How is cholera spread?

A

Faecal oral route - contaminated water/food

24
Q

What does cholera infection present with?

A

Severe dehydration secondary to diarrhoea, maybe vomiting, nausea, abdominal pain

25
Q

What diagnosis for cholera infection?

A
  • Bacterial culture from stool sample on selective agar,

- rapid dipstick tests available

26
Q

What treatment for cholera infection? what is the vaccine name?

A

Oral rehydration. Vaccine - dukoral (oral inactivated)

27
Q

What are other causes of infectious diarrhoea/gastroenteritis?

A
  1. Viral (rotavirus, norovirus)
  2. protozoal parasitic (giardia lambilia, enamoeba histiolytica)
  3. bacterial (campylobacter jejuni, E.coli, salmonella, shigella, c.diff)
28
Q

How do rotaviruses work? What are the types? What is treatment? Who does it commonly infect?

A
  • RNA virus replicated in enterocytes.
  • 5 types A-E, E most common in humans.
  • Most common cause of diarrhoea in infants and young kids.
  • Supportive treatment - oral rehydration.
  • Vaccine rotarix - live attentuated oral vaccine against type A
29
Q

what is the most common cause of diarrhoea in infants & young kids?

A

rotavirus

30
Q

How does norovirus infect people? Mode of transmission? Incubation period? How long can remain infectious for? Where do these outbreaks usually happen? Treatment? Diagnosis?

A
  • RNA virus.
  • Faecal oral route.
  • Incubation 24-48h. Can remain infectious up to 2 weeks.
  • Outbreaks in closed communities.
  • Acute gastroenteritis recovery 1-3 days no treamtent usually.
  • Diagnosis via sample PCR
31
Q

What causes campylobacter transmission? Treatment? Resistance?

A
  • Undercooked meet (especially poultry), untreated water and unpasteurised milk.
  • Low infective dose (few bacteria can cause illness).
  • Treatment not usually needed but azithromycin standard.
  • Resistant to fluoriquinones.
  • Common cause of food poisoning
32
Q

What are E.coli features? What are the 6 pathotypes associated with diarrhoea and what do they cause?

A
  • Gram negative intestinal bacteria, most harmless.
    1. enterotoxigenic E.coli (ETEC): cholera-like toxin, watery diarrhoea
    2. enterohaemorrhagic or shiga-toxin producing (EHEC): some get haemolytic uraemic syndrome, loss of kidney function
    3. enteroinvasive E.coli (EIEC): shigella like illness, bloody diarrhoea.
  • Others - enteropathogenic, enteroaggregative, diffusely adherent
33
Q

What is management for C.diff infection?

A
  • Isolate patient, stop current antibiotics.
  • Use metronidazole, vancomycin.
  • Increasingly hard to treat with recurrence.
  • FMT (faecal microbiota transplantation) high cure rate.
34
Q

How does c.diff cause infection?

A
  • Usually associated with antibiotics use.

- Exists in gut in equilibrium, dysbiosis caused by antibiotics causes c.diff overgrowth - toxin production.

BRS (81 decks)

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