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1B Gastroenterology > Immunology of the Gut > Flashcards

Immunology of the Gut Flashcards

1
Q

what is the antigen load of the gut provided by?

A

resident microbiota bacteria

dietary antigens

exposure to pathogens

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2
Q

what is the active stage of the gut?

A

state of restrained activation:

  • tolerance vs active immune response

tolerance (food antigens & commensal bacteria)

immunoreactivity (pathogens)

  • dual immunological role
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3
Q

what is required for immune homeostasis of gut and health immune system

A

bacterial microbiota presence

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4
Q

what are the 4 major phyla of bacteria?

A

bacteroidetes

firmicutes

actinobacteria

proteobacteria

(also viruses and fungi)

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5
Q

how does the host increase and decrease bacterial cell numbers?

A
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6
Q

what is the site of immunological defect with development of small intestine?

A

peyers patches- fewer and less cellular

lamina propria- thinner and less cellular

germinal centres- fewer plasma cells

isolated lymphoid follicles- smaller and less cellular

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7
Q

where does an immunological defect with development of mesenteric lymph nodes affect?

A

germinal centres- smaller, less cellular with fewer plasma cells

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8
Q

what is the location of an immunological defect of CD8 T-cells?

A

intestinal epithelial lymphocytes- fewer cells with reduced cytotoxicity

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9
Q

what defects can affect the intestine epithelial cells and reduce them?

A

immunological defect with:

  • expression MHC class II molecules

expression of TLR9

levels of IL-25

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10
Q

what location do immunological defects with expression of angiotensin 4 and REG3y affect?

A

paneth cells

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11
Q

what location does immunological defect in production of secretory IgA affect?

A

B cells

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12
Q

what location does an immunological defect with CD4 T cells affect?

A

lamina propria- fewer cells, decreased Th cells in small intestine and increased in colon

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13
Q

what location does an immunological defect with CD4-CD25 T cells affect?

A

mesenteric lymph nodes- reduce expression FOXP3 and reduces suppressive capacity

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14
Q

what are the chemical digestive factors produced and bacterial content for different areas of GI tract?

A
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15
Q

what is symbiosis?

A

living together with no harm/gain

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16
Q

what is commensal?

A

microorganisms that benefit from host but has no effects on the host

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17
Q

what is pathobionts?

A

symbiosis with inflammatory response under right environment

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18
Q

what is dysbiosis?

A

immunological disequilibrium with sway to produce pathogens -> pathobionts inflammation

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19
Q

what are the causes of dysbiosis?

A

infection/ inflammation

diet

xenobiotics

hygiene

genetics

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20
Q

what are the physical barriers in mucosal defense?

A

anatomical= epithelial barries & peistalsis

chemical= enzymes & acidic pH

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21
Q

what are the different layers to the epithelial barrier?

A

mucus layer- goblet cells

epithelial monolayer- tight junctions

paneth cells (small intestine)

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22
Q

where are paneth cells located?

A

bases of crypts of Lieberkuhn

secrete antimicrobial peptides (defensins) and lysozyme

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23
Q

what is the effect of commenal bacterial in mucosal defence?

A

ecological barrier

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24
Q

what is the immunological response following invasion?

A
  • MALT (mucosa associated lymphoid tissue)
  • GALT (gut associated lymphoid tissue)
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25
Q

where is MALT located?

A

found in submucosa below the epithelium, as lymphoid mass containing lymphoid follicles

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26
Q

what are MALT follicles surrounded by?

A

HEV postcapillary venules, allowing easy passages of lymphocytes

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27
Q

what is the level of immunological tissue in the oral cavity?

A

rich

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28
Q

what is GALT responsible for?

A
  • adaptive & innate immune responses
  • Consists of B & T lymphocytes, macrophages, APC (dendritic cells), and specific epithelial & intra-epithelial lymphocytes
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29
Q

what are the types of lymphoid tissue?

A

non- organised

organised

30
Q

what are the types of non-organised GALT?

A
  • Intra-epithelial lymphocytes
    • Make up 1/5th of intestinal epithelium, e.g. T-cells, NK cells
  • Lamina propria lymphocytes
31
Q

what are the types of organised lymphoid tissue?

A
  • Peyer’s patches (small intestine)
  • Caecal patches (large intestine)
  • Isolated lymphoid follicles
  • Mesenteric lymph nodes (encapsulated)
32
Q

what are non-organised GALT?

A

stem cells which produce enterocytes

33
Q

how do non-organised GALT reproduce in the small and large intestine?

A
  • migrate to APEX
  • form apoptotic intraepithelial cells
  • At base also get goblet cells formed and move up to produce mucous
  • Stem cells also produce Paneth cells which produce anti-microbial peptides
  • Within the epithelium have intraepithelial lymphocytes
  • Within lamina propria have intestinal immune cells (T-cells, B-cells, macrophages and dendritic cells)
  • The large intestine doesn’t have:
    • Paneth cells (lots goblet cells)
    • Villi (only crypts)
  • the large intestine has intraepithelial lymphocytes
34
Q

where are Peyer’s patch located?

A
  • Found in submucosa small intestine – mainly distal ileum
35
Q

what is the composition of Peyer’s patch?

A
  • Aggregated lymphoid follicles covered with follicle associated epithelium (FAE).
  • FAE - no goblet cells, no secretory IgA, no microvilli
  • Organised collection of naïve T cells & B-cells
  • Development requires exposure to bacterial microbiota
    • 50 in last trimester foetus, 250 by teens
  • Antigen uptake via M (microfold) cells within FAE
  • M cells express IgA receptors
    • facilitating transfer of IgA-bacteria complex into the Peyer’s patches.
36
Q

what is the use of trans-epithelial dendritic cells?

A

way to get bacteria into cell without use of M cells

37
Q

how do trans-epithelial dendritic cells work?

A
  • open-up tight junction proteins and send dendrites outside epithelium
  • sample bacteria and bring it back to process and transport to mesenteric lymph nodes
  • have tight junction proteins to maintain integrity of epithelial barrier once they have taken antigen from lumen of gut
38
Q

how does the B cell adaptive response work?

A
  • Mature naïve B-cells express IgM in Peyer’s Patches
  • On antigen presentation class switches to IgA
  • T-cells & epithelial cells influence B cell maturation via cytokine production
  • B cells further mature to become IgA secreting plasma cells.
  • Populate lamina propria
39
Q

how is secretory IgA produced?

A
  • plasma cells migrate to enterocytes
  • Taken up into epithelial cells
  • Undergo enzymatic cleavage
  • Secreted as secretory IgA
40
Q

what are the effects of sIgA?

A

binds to luminal antigen

preventing its adhesion and consequent invasion

41
Q

how does lymphocytes homing and circulation occur?

A
  1. peyer’s patch-antigen presentation & activation
  2. mesenteric lymph node (lymphocyte proliferation)
  3. thoracic duct
  4. circulation

5 lamina propria or peripheral immune system

42
Q

where does 𝝰4β7 Integrin/MAdCAM-1 Adhesion & Gut Homing occur?

A
  • high endothelial venules
    • Express mucosal addressin cell adhesion molecule 1 (MAdCAM1)
  • Lymphocytes express 𝝰4β7 Integrin
  • Lymphocytes roll along HEV until tethered by activation MAdCAM1
  • Rolling arrests and migrate into lamina propria
  • B-Cells do the same thing
43
Q

what is the life span of enterocytes and goblet cells?

A
  • Enterocytes & goblet cells of small bowel have a short life span (about 36 hrs)
  • Rapid turnover contrasts with lifespan of weeks/months for other epithelial cell types (e.g. lung, blood vessels)
44
Q

why do enterocytes have such a high turn over?

A
  • Enterocytes are first line of defense against GI pathogens & may be directly affected by toxic substances in diet.
  • Effects of agents which interfere with cell function, metabolic rate etc will be diminished.
  • Any lesions will be short-lived.
45
Q

what is the cholera infection mechanism?

A
  • acute bacterial disease caused by Vibrio cholerae serogroups O1 & O139
  • Bacteria reaches small intestine → contact with epithelium & releases cholera enterotoxin.
  • Toxin internalised through retrograde endocytosis
  • Causes activation adenylate cyclase and cAMP
  • Active secretion salt and fluid through activation of cystic fibrosis transmembrane conductance regulator (CFTR)
  • High loss salt, potassium, chloride, bicarb
  • Water follows this concentration gradient causing diarrhoea
46
Q

what is the transmission of cholera?

A

faecal-oral route

mainly spreads via contaminated water & food

47
Q

main symptoms of cholera?

A

severe dehydration & water diarrhoea

other symptoms:

vomiting, nausea and abdo pain

48
Q

how is cholera diagnosed?

A

bacterial culture from stool sample on selective agar is the gold standard, rapid dipstick tests also available.

49
Q

what is the treatment for cholera?

A

oral-rehydration is the main management ; up to 80% of cases can be successfully treated.

50
Q

what is the prevention for cholera?

A

vaccine

Dukoral, oral, inactivated.

51
Q

what are the viral causes of infectious diarrhoea?

A
  • Rotavirus (children)
  • Norovirus “winter vomiting bug”
52
Q

what are the bacterial causes of infectious diarrhea?

A
  • Campylobacter jejuni
  • Escherichia coli
  • Salmonella
  • Shigella
  • Clostridium difficile
53
Q

what are the protozoal parasitic causes of infectious diarrhoea?

A
  • Giardia lamblia
  • Entamoeba histolytica
54
Q

what are rotaviruses?

A
  • RNA virus, replicates in enterocytes.
  • 5 types A – E, type A most common in human infections.
55
Q

what is the main cause of diarrhoea in infants and young children worldwide?

A

rotavirus

56
Q

what is the treatment for rotavirus?

A

oral rehydration therapy

57
Q

what is the prevention for rotavirus?

A

vaccination- live attenuated oral vaccine (Rotarix) against type A

before vaccine, most individuals infected by age 5, repeated infections develop immunity

58
Q

what type of virus is norovirus?

A
  • RNA virus
  • Incubation period 24-48 hours
59
Q

what is the transmission of norovirus?

A
  • Faecal-oral transmission.
  • Individuals may shed infectious virus for up to 2 weeks
  • Outbreaks often occur in closed communities
60
Q

what are the symptoms of norovirus?

A
  • Acute gastroenteritis, recovery 1 – 3 days
61
Q

what is the treatment of norovirus?

A

not usually required

62
Q

what is the diagnosis of norovirus?

A

simple PCR

63
Q

what are the most common species of campylobacter?

A
  • Campylobacter jejuni, Campylobacter coli
64
Q

what is the transmission of campylobacter?

A
  • Undercooked meat (especially poultry), untreated water & unpasteurised milk

Low infective dose, a few bacteria (<500) can cause illness

65
Q

what is the treatment of campylobacter?

A
  • Not usually required
  • Azithromycin (macrolide) is standard antibiotic
  • Resistance to fluoroquinolones is problematic
66
Q

what is the commonest cause of food poisoning in the UK

A

campylobacter

67
Q

what are the features of E.col?

A
  • Diverse group of Gram-negative intestinal bacteria
  • most harmless
  • 6 ”pathotypes” associated with diarrhea (diarrhoeagenic):
    • enterotoxigenic E.coli (ETEC)
    • enterohaemorrhagic or Shiga toxin-producing E.coli (EHEC/STEC)
    • enteroinvasive E.coli (EIEC)
    • enteropathogenic E.coli (EPEC)
    • enteroaggregative E.coli (EAEC)
    • diffusely adherent E.coli (DAEC)
68
Q

what are the features of ETEC?

(enterotoxigenic E.coli)

A
  • Cholera like toxin
  • Watery diarrhoea
69
Q

what is a consequence of Enterohaemorrhagic E.coli (EHEC/STEC)?

A

haemolytic uraemic syndrome: loss kidney funciton

70
Q

what are the features of Enteroinvasive E.coli (EIEC)

A

shigella like illness

bloody diarrhoea

71
Q

what is the management of C.DIff?

A
  • Isolate patient (very contagious)
  • Stop current antibiotics
  • Metronidazole, Vancomycin
  • Recurrence rate 15-35% after initial infection, increasingly difficult to treat.
  • Faecal Microbiota Transplantation (FMT) – 98% cure rate
72
Q

how does C. Diff occur?

A
  1. microbiota of healthy human can contain c.diff without problems
  2. Dysbiosis (usually caused by exogenous disturbance (antibiotics))
  3. C. diff starts colonising enterocytes in gut but not producing any toxin
  4. Pathogen induced disturbance crease supportive environment to produce a toxin= inflammation distal gut
  5. Metronidazole can cause c.diff as well as treating it!

1B Gastroenterology (12 decks)

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