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BRS Year 2 > gut immunology > Flashcards

gut immunology Flashcards

1
Q

what does it mean that the gut is in a state of restrained activatiom?

A

dual immunological role between tolerance and active immune response

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2
Q

what are the major phyla of gut bacteria?

A

bacteriodetes
firmicutes
actinobacteria
proteobacteria

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3
Q

host factors influencing bacterial cell numbers

A

nutrients (bacterial growth)

digestive factors, peristalsis, defecation (elimination of bacteria)

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4
Q

where is gut bacteria most prevalent and why?

A

colon

no digestive factors so numbers highest here, increases along tract

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5
Q

what is dysbiosis?

A

microbial imbalance (pathobionts and symbionts)

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6
Q

causes of dysbiosis?

A 
infection and inflammation
diet
xenobiotics
hygiene
genetics
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7
Q

types of anatomical mucosal defences in GI tract

A

Epithelial barrier

Peristalsis

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8
Q

factors produced by pathobionts contributing to disease development

A

TMAO
4-EPS
SCFAs
AHR ligands

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9
Q

what is the bacterial factor TMAO indicated in?

A

increased cholesterol deposition so athersclerosis

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10
Q

what are the chemical mucosal defences against pathogens in GI tract

A

Enzymes

Acidic pH

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11
Q

how do commensal bacteria form a mucosal defence?

A

occupy an ecological niche

act as second line to anatomical/chemical defences

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12
Q

what are the immunological mucosal defences of GI tract?

A

MALT (Mucosa Associated Lymphoid Tissue)

GALT (Gut Associated Lymphoid Tissue)

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13
Q

how does the epithelial barrier protect against infection?

A

mucus layer produced by goblet cells
tight junctions between epithelium
paneth cells (small intestine)

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14
Q

what is the role of paneth cells and their location?

A

small intestine, bases of crypts of Lieberkuhn

secrete antimicrobial peptides and lysozyme

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15
Q

what are MALTs?

A

mucosa associated lymphoid tissue esp in oral cavity

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16
Q

structure and location of MALTs?

A

below epithelium as a mass of lymphoid follicles
surrounded by high endothelial venules allowing easy passage of lymphocytes
oral cavity; linguinal tonsils, palatine tonsils, adenoid tonsils

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17
Q

what are GALTs?

A

gut associated lymphoid tissue
responsible for GI tract adaptive and innate response - B&T cells, macrophages, DCs, specific epithelial and intra-epithelial lymphocytes

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18
Q

what are organised GALTs?

A

peyers patches - distal ileum
caecal patches- large intestine
isolated lymphoid follicles
mesenteric lymph nodes

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19
Q

location of peyers patches?

A

distal ileum

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20
Q

what are non-organised GALTs?

A

intraepithelial lymphocytes

lamina propria lymphocytes

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21
Q

what are the nonorganised GALTs of small intestine?

A

intraepithelial lymphocytes - antimicrobial peptides
goblet cells
paneth cells
lamina propria

22
Q

what are the non organised GALTs of large intestine?

A

goblet cells
intraepithelial lymphocytes

no paneth cells like small i

23
Q

describe structure of peyers patches

A

aggregated lymphoid follicles underneath FAE (follicle associated epithelium) and M cells
sub epithelial dome of dendritic cells
B cells in follicle
naive t cells surround B cells

24
Q

what are M cells in peyers patches?

A

microfold cells
antigen uptake through them via IgA receptors
allow IgA-bacteria complexes to enter peyers patches

25
Q

what are follicle associated epithelial cells?

A

cells overlying peyers patches

have no microvilli, goblet cells or IgA

26
Q

how can antigen sampling occur in the GI tract

A

via M cells

OR independent of M cells by transepithelial dendritic cells

27
Q

how do transepithelial dendritic cells sample antigens?

A

can open tight junction proteins and send dendrites to lumen of gut
directly samples the bacteria and can transfer to mesenteric lymph nodes

28
Q

describe the B cell adaptive response in the gut/GALT

A

mature (but naive) B cells express IgM
on antigen presentation, class switch to IgA
T cells and epithelial cells produce cytokines to influence maturation
B cells then mature to be IgA producing plasma cells
plasma cells then migrate and populate lamina propria

29
Q

how does secretory IgA help immunological defence of gut

A

sIgA binds to luminal antigen, prevents adhesion and consequent invasion

30
Q

how can circulating lymphocyte reenter intestinal GALTs?

A

process of lymphocyte homing

31
Q

where do GALT lymphocytes travel after activation?

A

mesenteric lymph nodes
to enter thoracic duct, enter broad circulation
from there return to lamina propria (via lymphocyte homing)
or move to peripheral lymph tissue

32
Q

what is peripheral lymph tissue?

A

skin
tonsils
BALTs - bronchus associated lymphoid tissue

33
Q

what is the process of lymphocyte homing?

A

lymphocytes in HEVs
MAdCAM-1 on HEVs binds to lymphocyte 𝝰4β7 Integrin
lymphocytes roll until tethered by MAdCAM-1 for activation and rolling arrest
move through walls to lamina propria

34
Q

why is there rapid turnover of enterocytes?

A

first line of defence - may be directly affected by toxic substances in diet
therefore any agents affecting cell function die off and effect is diminished
therefore any lesions will be short lived and not have long lasting effects

35
Q

what bacteria is cholera caused by incl serotype

A

vibrio cholerae O1 and O139

36
Q

MOA of cholera infection

A

Bacteria reaches small intestine → contact with epithelium & releasescholera enterotoxin
enterotoxin internalised via retrograde endocytosis
causes activation of adenylate cyclase to increase cAMP
causes active secretion of salt and fluid (via CFTR)
leads to watery diarrhoea via osmosis

37
Q

transmission of cholera

A

faecal oral route - contaminated food and water

38
Q

symptoms of cholera

A

severe dehydration and watery diarrhoea
vomiting
nausea
abdo pain

39
Q

how to diagnose cholera

A

bacterial culture of stool sample

rapid dipstick also available

40
Q

what protections are there against cholera

A

vaccine - oral inactivated (Dukoral)

41
Q

what viruses cause gastroenteritis

A

rotavirus in children

noravirus

42
Q

rotavirus treatment (gastroenteritis)

A

oral rehydration therapy

43
Q

what are rotaviruses

A

RNA viruses
replicate in enterocytes
subtypes A-E
live attenuated vaccine against type A (most common)

44
Q

what are noroviruses

A

RNA viruses
faecal oral transmission
usually outbreak in closed communities (cruises)
cause acute gastroenteritis symptoms - recovery 1-3 days

45
Q

what is the treatment for norovirus gastroenteritis

A

none required

46
Q

what is campylobacter gastroenteritis

A

commonest UK cause of food poisoning
low dose required for illness
treatment typically not required

47
Q

which pathogens causing gastroenteritis typically require no treatment?

A

campylobacter
norovirus
some e coli

48
Q

clostridium difficle gastroenteritis facts

A

often due to long term antibiotics
very contagious - isolate patient
start metronidazole/vancomycin

49
Q

treatments for clostridium difficile

A

metronidazole or vancomycin
stop current antibiotics
can give faecal microbiota transplantation

50
Q

pathotypes of e coli causing diarrhoea

A 
enterotoxigenic
enterohaemorrhagic
enteroinvasive
enteropathogenic
enteroaggregative
diffusely adherent
51
Q

transmission of campylobacter

A

undercooked meat esp poultry
untreated water
unpasteurised milk

BRS Year 2 (67 decks)

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