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brs (phase 1b) > (gastro) gut immunology > Flashcards

(gastro) gut immunology Flashcards

1
Q

what is the surface area of the GI tract?

A

approx 200 square metres

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2
Q

explain why the GI tract is said to have a massive antigen load

A

resident microbiota = 10^14 bacteria

dietary antigens

exposure to pathogens

= collectively result in an a huuuge antigen load

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3
Q

what is microbiota?

A

mixture of microorganisms that make up a community in an environmental niche

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4
Q

what is the microbiome?

A

collective genomes of all the microbiota

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5
Q

differentiate between microbiota and microbiome

A

microbiota = mixture of microorganisms that make up a community in an environmental niche

microbiome = collective genomes of all the microbiota

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6
Q

explain why the GI tract is in a state of ‘restrained activation’

A

has to balance tolerance of food antigens and commensal bacteria with the active immune response against foreign pathogens

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7
Q

why is bacterial microbiota important?

A

for the immune homeostasis of the gut and the development of a healthy immune system

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8
Q

how much gut bacteria is present in our body?

A

approx 10^14 gut bacteria

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9
Q

what makes up the gut microbiota?

A

four major phyla of bacteria (Bacteroidetes, Firmicutes, Actinobacteria, Proteobacteria), also viruses & fungi

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10
Q

what does the gut microbiota provide?

A

provide traits we have not had to evolve on our own

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11
Q

how is bacterial growth stimulated by the host?

A

via ingested nutrients or secreted nutrients

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12
Q

how is bacterial lysis/elimination stimulated by the host?

A

via chemical digestive factors

OR

via peristaltic contractions and defecation

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13
Q

which host actions lead to an increase in cell numbers?

A

ingested nutrients or secreted nutrients

= bacterial growth

= increased bacterial cell numbers

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14
Q

which host actions lead to a decrease in cell numbers?

A

chemical, digestive factors + peristaltic contractions + defecation

= bacterial lysis and elimination

= decreased bacterial cell numbers

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15
Q

why are microbiota important to the host?

A

provide essential nutrients

metabolise indigested components

defence against colonisation by opportunistic pathogens,

contribute to intestinal architecture

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16
Q

what is the effect of ingested/secreted nutrients in the gut microbiota?

A

stimulate bacterial growth

= increased bacterial cell numbers

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17
Q

what is the effect of chemical digestive factors in the gut microbiota?

A

stimulate bacterial lysis

= decreased bacterial cell numbers

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18
Q

what is the effect of peristalsis, contractions and defecation in the gut microbiota?

A

stimulate bacterial elimination

= decreased bacterial cell numbers

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19
Q

what chemical, digestive factors are produced by the host in the stomach, and what is the impact of this?

A

hydrochloric acid (pH 1-4)
pepsin
gastric lipase

= chemical, digestive factors that stimulate bacterial lysis and therefore decrease bacterial cell numbers

(10^1)

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20
Q

what chemical, digestive factors are produced by the host in the liver and what is the impact of this?

A

bile acids

= stimulate bacterial growth and therefore result in increased bacterial cell numbers

(10^3)

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21
Q

what chemical, digestive factors are produced by the host in the pancreas, and what is the impact of this?

A

trypsin
amylase
carboxypeptidase

= secreted nutrients that stimulate bacterial growth and therefore increase bacterial cell number

(10^4)

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22
Q

what chemical, digestive factors are produced by the host in the small intestine, and what is the impact of this?

A

brush border enzymes

= increase bacterial content

(10^7)

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23
Q

what chemical, digestive factors are produced by the host in the colon, and what is the impact of this?

A

no host digestive factors

= reduced bacterial lysis
= bacterial cell numbers cannot remain decreased
= huuuge increase in colonic bacteria

(10^12)

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24
Q

define symbiosis

A

any relationship or interaction between two dissimilar organisms (not always to the mutual benefit of either species)

the specific kind of symbiosis depends on whether either or both organisms benefit from the relationship

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25
Q

define dysbiosis

A

reduction in microbial diversity

(a combination of the loss of beneficial bacteria + rise in pathobionts)

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26
Q

what are symbionts?

A

an organism living in symbiosis with another

(any kind of interaction between two dissimilar organisms)

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27
Q

what are commensals?

A

relationship between organisms where one organism benefits from the association while not harming the other

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28
Q

what are pathobionts?

A

any potentially pathological organism that, under normal circumstances, lives as a non-harming symbiont

(do have the potential to cause dysregulated inflammation and disease in specific environments)

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29
Q

what happens when pathobionts malfunction?

A

have the potential to cause dysregulated inflammation and disease

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30
Q

what are some possible causes of dysbiosis?

A

infection or inflammation

diet

xenobiotics

hygiene

genetics

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31
Q

which bacterial metabolites and toxins are produced as a result of dysbiosis?

A

TMAO
4-EPS
SCFA
bile acids
AHR ligands

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32
Q

what is the effect of the bacterial metabolite TMAO?

A

increase cholesterol deposition in the artery wall

= can lead to atherosclerosis

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33
Q

what is the effect of the bacterial metabolite SCFA?

A

short-chain fatty acids decrease and can cause IBD

if increase can cause neuropsychiatric disorders

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34
Q

what is the effect of the bacterial metabolite AHR ligands?

A

present in multiple sclerosis, rheumatoid arthiritis, asthma

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35
Q

which conditions can occur as a result of dysbiosis?

A
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36
Q

what are the physical barriers of mucosal defense?

A

anatomical = epithelial barrier, peristalsis

chemical = enzymes, acidic pH

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37
Q

what are the anatomical physical barriers?

A

epithelial barrier, peristalsis

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38
Q

what are the chemical physical barriers?

A

enzymes, acidic pH

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39
Q

what are the immunological barriers of mucosal defense?

A

MALT (mucosa associated lymphoid tissue)

GALT (gut associated lymphoid tissue)

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40
Q

summarise the barriers for mucosal defense in the body

A
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41
Q

explain how the epithelium acts as a barrier

A

has a mucus layer (secreted by goblet cells) = to trap pathogens

has tight junctions (within the epithelial monolayer) = prevent barrier intrusion by pathogens into the epithelium

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42
Q

how is the epithelium of the small intestine specialised for mucosal defense?

A

contains Paneth cells in the bases of the crypts of Lieberkuhn

= secrete antimicrobial peptides (defensins) and lysozyme

(and mucus layer + tight junction of the epithelial monolayer)

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43
Q

what happens if the physical barriers for mucosal defense fail?

A

rely on the immunological barriers (MALT, GALT)

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44
Q

what is MALT?

A

mucosa-associated lymphoid tissue

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45
Q

what is GALT?

A

gut-associated lymphoid tissue

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46
Q

where are Paneth cells found?

A

in the bases of the crypts of Lieberkuhn of the small intestine

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47
Q

why are Paneth cells important?

A

secrete antimicrobial peptides (defensins) & lysozyme

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48
Q

where is MALT found?

A

found in the submucosa below the epithelium

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49
Q

how is MALT structured?

A

as lymphoid mass containing lymphoid follicles

follicles are surrounded by HEV postcapillary venules, allowing easy passage of lymphocytes

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50
Q

how are MALT follicles arranged?

A

surrounded by HEV postcapillary venules, allowing easy passage of lymphocytes

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51
Q

what are HEV postcapillary venules?

A

high endothelial venules

(postcapillary venules)

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52
Q

how are HEV postcapillary venules structured?

A

plump endothelial cells as opposed to the usual thinner endothelial cells found in regular venules

= enable lymphocytes circulating in the blood to directly enter a lymph node (by crossing through the HEV)

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53
Q

why are HEV postcapillary venules important?

A

enable lymphocytes circulating in the blood to directly enter a lymph node (by crossing through the HEV)

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54
Q

which cavity is rich in MALT?

A

oral cavity (rich in immunological tissue)

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55
Q

what is GALT responsible for?

A

responsible for both adaptive & innate immune responses

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56
Q

what does GALT consist of?

A

consists of B & T lymphocytes, macrophages, APC (dendritic cells), and specific epithelial & intra-epithelial lymphocytes

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57
Q

what are the two types of GALT?

A

non-organised GALT
organised GALT

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58
Q

what is non-organised GALT?

A

intraepithelial lymphocytes (make up 1//5th of the intestinal epithelium = T cells, NK cells)

lamina propria lymphocytes

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59
Q

what are intra-epithelial lymphocytes?

A

make up 1//5th of the intestinal epithelium = T cells, NK cells

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60
Q

what is organised GALT?

A

Peyer’s patches (small intestine)

caecal patches (large intestine)

isolated lymphoid follicles

mesenteric lymph nodes (encapsulated)

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61
Q

how does GALT compare to other lymphoid tissue?

A

largest part of lymphoid tissue in the body

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62
Q

what is the effect of the bacterial metabolite 4-EPS?

A

associated w autism

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63
Q

where are intra-epithelium lymphocytes found?

A

slotted in between the enterocytes of the small intestine
(approx 1/5th of the intestinal epithelium)

= include T cells and NK cells

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64
Q

what are the most common cell types to develop from the stem cells in the crypts of Lieberkuhn?

A

intestinal epithelial cells (enterocytes)

migrate to the tip of the villi

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65
Q

what types of cells are produced by the stem cells in the crypts?

A

absorptive enterocytes

mucus-secreteing goblet cells

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66
Q

where do Paneth cells migrate to?

A

to the bottom of the crypt

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67
Q

what is the characteristic feature of Paneth cells?

A

contain antimicrobial peptides (defensins) = dense granules

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68
Q

what makes up the central part of the villus?

A

lamina propria

= containing the majority of the intestinal cells (T cells, dendritic cells, macrophages)

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69
Q

where are Peyer’s patches found?

A

found in submucosa small intestine – mainly distal ileum

70
Q

describe the structure of a Peyer’s patch

A

aggregated lymphoid follicles covered with follicle associated epithelium (FAE)

71
Q

what is FAE?

A

follicle associated epithelium

= organised collection of naive T and B cells

72
Q

what are the features of FAE?

A

no goblet cells

no secretory IgA

no microvilli

73
Q

what does FAE contain?

A

naive T and B cells

74
Q

how do Peyer’s patches develop?

A

requires exposure to bacterial microbiota

75
Q

how do Peyer’s patches change with age?

A

(50 in last trimester foetus, 250 by teens)

= increase with age

76
Q

what is Peyer’s patch function linked to?

A

linked to M cells that Peyer’s patches lie beneath

77
Q

what are M cells?

A

microfold cells

= responsible for transporting antigens from the lumen into the Peyer’s patches

78
Q

where are M cells found?

A

found above the Peyer’s patches

79
Q

what is the function of the M cells?

A

responsible for antigen uptake within FAE

= they express IgA receptors, facilitating the transfer of IgA-bacteria complex into the Peyer’s patches

80
Q

which immunoglobulin is linked to M cell function?

A

M cells have IgA receptors

= facilitate the transport of IgA bacterial complexes into the Peyer’s patches

81
Q

how are M cells different to the normal small intestine?

A

M cells have surface microfolds and not microvillii

= antigens are preferentially taken up by M cells

82
Q

what is the alternative route for bacterial invasion, independent of M cells?

A

using trans-epithelial dendritic cells

= send their dendrites out of the lamina, past the tight junction of the epithelial monolayer, into the gastrointestinal lumen to sample the bacteria and transport it back to the mesenteric lymph node

83
Q

how do trans-epithelial dendritic cells sample antigens in the lumen?

A

send their dendrites out of the lamina

past the tight junction of the epithelial monolayer

into the gastrointestinal lumen to sample the bacteria

and transport it back to the mesenteric lymph node

84
Q

where are the antigens sampled by the trans-epithelial dendritic cells taken to?

A

mesenteric lymph node

85
Q

explain the B cell adaptive immune response in the small intestine

A

pathogens taken up by M cells

antigen excreted into pockets in the inner surfaces of enterocytes that contain APCs (dendritic cells)

the APCs (dendritic cells) engulf antigens and present them on their surface MHC II to T cells

dendritic cells then migrate to the Peyer’s patches and then APCs, T cells and B cells all aggregate in the patch and form organsied lymphoid follicle

other dendritic cells migrate through lymphatic system and activate T cells, B cells and other plasma cells in the mesenteric lymph node in the lamina propria

some of these activated cells can return to GALT effector sites (e.g. enterocyte lining) and produce antibodies secreted from the intestinal lumen

86
Q

which immunoglobulin do the mature B cells in Peyer’s patches express?

A

IgM

87
Q

how does the immunoglobulin presented by mature B cells in the Peyer’s patch change?

A

mature, naive B cells in the Peyer’s patch present IgM initially

and upon antigen presentation, they switch to expressing IgA

88
Q

why do mature B cells switch to presenting IgA?

A

due to antigen presentation in the Peyer’s patch

89
Q

what is B cell maturation affected by in the intestinal submucosa and how?

A

affected by T cells and epithelial cells that influence B cell maturation via cytokine production

90
Q

what do mature B cells further become in the intestinal submucosa?

A

IgA-secreting plasma cells

91
Q

which region are Peyer’s patches, B cells and Tcells found in the intestinal tract?

A

lamina propria

92
Q

how are pathogens processed by antigen-presenting cells in the lamina propria of the GI tract?

A

the APC in usually a dendritic cell

engulf antigen and present it on their surface via MHC II molecules

(to T cells, B cells in the Peyer’s patch)

93
Q

what are GALT tissue effector sites and what happens here?

A

the intestinal enterocyte lining

(where secretory IgA is released into the intestinal lumen)

94
Q

what are the two paths an APC can take during the B cell adaptive response?

A
  • either migrate to Peyer’s patches and accumulate with T cells and B cells to form an organised lymphoid follicle
  • travel through the lamina propria activating immune cells
95
Q

how is secretory IgA formed?

A

plasma cells in the intestinal submucosa secrete IgA

the IgA is taken up by enterocytes via the IgA receptor and engulfed in a vesicle

enzymatic cleavage takes place

secretory IgA is released into the lumen

96
Q

how much of the gut is involved in IgA secretion?

A

up to 90% of gut B-cells secrete IgA

97
Q

what is the purpose of secretory IgA?

A

binds to luminal antigens

= preventing their adhesion and consequent invasion

98
Q

explain the process of lymphocyte homing

A

travel from the Peyer’s patches to the mesenteric lymph node for lymphocyte proliferation

return to circulation via the thoracic duct

when in circulation, follow one of two paths:

a) enter the peripheral immune system (e.g. skin, tonsils, BALT)
b) return to the intestinal mucosa and lamina propria

99
Q

why do lymphocytes migrate to the mesenteric lymph node?

A

for lymphocyte proliferation

100
Q

what are the two possible pathways after the lymphocyte enters circulation?

A

when in circulation, follow one of two paths:

a) enter the peripheral immune system (e.g. skin, tonsils, BALT)
b) return to the intestinal mucosa and lamina propria

101
Q

what are examples of structures that constitute the peripheral immune system?

A

e.g. skin, tonsils, BALT

102
Q

what is BALT?

A

bronchus-associated lymphoid tissue

103
Q

what happens at the Peyer’s patches?

A

antigen presentation and immune cell activation

104
Q

explain how lymphocytes return to the lamina propria in lymphocyte homing

A

in the HEVs, MAdCAM-1 is expressed on the surface

the lymphocytes express a4B7

lymphocytes rolling along the HEV and then the MAdCAM-1 and a4B7 interact

resultant chemotactic stimulation results in antigen activation and internalisation of the T cell back into the lamina propria

105
Q

what is MAdCAM-1?

A

lymphocyte homing into the intestine is mediated by binding of lymphocytes to mucosal addressin cell adhesion molecule 1 (MAdCAM-1), expressed on endothelial cells

106
Q

where is MAdCAM-1 expressed?

A

expressed on endothelial cells of HEVs (high endothelial venules)

107
Q

what does MAdCAM-1 interact with?

A

interacts with a4B7-integrin on the surface of lymphocytes

108
Q

what is a4B7-integrin?

A

cell adhesion molecule expressed on lymphocyte cell membranes that recognise addressing (MAdCAM-1) on target endothelial tissues

109
Q

where is a4B7-integrin expressed?

A

expressed on lymphocyte cell membranes

110
Q

what does a4B7 integrin and MAdCAM-1 interaction result in?

A

internalisation of the lymphocyte back into the lamina propria of the intestine

= lymphocyte homing into the intestine

111
Q

what is the life span of enterocytes and goblet cells of the small intestine and how does this compare to that of other cells?

A

have a short life span of about 36 hours

= this rapid turnover contrasts with life span of weeks/months for other epithelial cell types (e.g. lung, blood vessels)

112
Q

why is there a rapid turnover for enterocytes?

A

enterocytes are the first line of defense against GI pathogens and may be directly affected by toxic substances in the diet

= so if any agents interfere with enterocyte cell function, the effect of that interference will be reduced due to the short life span

113
Q

why is the rapid enterocyte turnover physiologically useful?

A

effects of agents which interfere with cell function and metabolic rate will be diminished

= any lesion will be short-lived

114
Q

what is cholera infection?

A

acute bacterial disease

115
Q

which microbe(s) causes cholera?

A

Vibrio cholerae serogroups O1 & O139

116
Q

explain the mechanism of action of cholera infection

A

bacteria enters the small intestine and come into contact with the epithelium and releases the cholera enterotoxin

cholera enterotoxin becomes internalised via retrograde endocytosis

= increased adenylate cyclase activity
= increased levels of cAMP
= increased active secretion of salts into the GI lumen
= water follows in large amounts due to the extremely steep osmotic gradient
= watery diarrhoea

117
Q

how does the cholera toxin become internalised?

A

becomes internalised via retrograde endocytosis

118
Q

what occurs as a result of cholera enterotoxin internalisation?

A

stimulates increased adenylate cyclase activity

= increased levels of cAMP
= increased active secretion of salts into the GI lumen

119
Q

what is the impact of increased luminal salt secretion?

A

= increased active secretion of salts into the GI lumen
= water follows in large amounts due to the extremely steep osmotic gradient
= watery diarrhoea

120
Q

what structure enables the active secretion of salt?

A

activation of CFTR (cystic fibrosis transmembrane regulator)

121
Q

how is cholera infection transmitted?

A

transmitted through faecal-oral route

= spreads via contaminated food & drink

122
Q

what are the main symptoms of cholera infection?

A

severe dehydration secondary to watery diarrhoea

123
Q

why is watery diarrhoea caused by cholera infection?

A

internalisation of the cholera enterotoxin into the small intestine

= increased adenylate cyclase activity
= increased levels of cAMP
= increased active secretion of salts into the GI lumen
= water follows in large amounts due to the extremely steep osmotic gradient
= watery diarrhoea

124
Q

what are the general symptoms of cholera infection?

A

vomiting, nausea & abdominal pain

125
Q

how is cholera infection diagnosed?

A

bacterial culture from stool sample on selective agar

(rapid dipstick tests also available)

126
Q

how is cholera infection treated?

A

oral-rehydration is the main management

127
Q

which vaccines are available to target cholera infection?

A

oral, inactivated vaccine = Dukoral

128
Q

what is the global epidemiology of cholera like?

A

globally 1.3 - 4 million cases, avg. 95,000 deaths/year

129
Q

which salts are actively secreted as a result of cholera infection?

A

Na+. K+, Cl-, HCO3-

130
Q

what are viral causes of gastroenteritis (i.e. infectious diarrhoea)?

A

rotavirus (children)

norovirus “winter vomiting bug”

131
Q

what are bacterial causes of gastroenteritis (i.e. infectious diarrhoea)?

A

Campylobacter jejuni
Escherichia coli
Salmonella
Shigella
Clostridium difficile

132
Q

what are protozoal parisitic causes of gastroenteritis (i.e. infectious diarrhoea)?

A

Giardia lamblia
Entamoeba histolytica

133
Q

what are rotaviruses?

A

RNA viruses that replicate in enterocytes

134
Q

where do rotaviruses replicate?

A

in enterocytes

135
Q

how many types of rotaviruses are there?

A

= 5 types A – E, type A most common in human infections

136
Q

who is most affected by rotaviruses?

A

most common cause of diarrhoea in infants & young children worldwide

137
Q

how is rotavirus infection treated?

A

oral rehydration therapy

138
Q

is a vaccination available against rotaviruses?

A

live, attenuated oral vaccine (Rotarix) against type A introduced in UK (July 2013)

(before introduction of vaccine, most children were affect before age 5 so their immunity consequently also developed)

139
Q

what are noroviruses?

A

RNA viruses

140
Q

what is ab incubation period?

A

the number of days between when you’re infected with something and when you might see symptoms

141
Q

what is the incubation period for noroviruses?

A

incubation period 24-48 hours

142
Q

how are noroviruses transmitted?

A

faecal-oral transmission

individuals may shed infectious virus for up to 2 weeks

143
Q

what happens with noroviruses in small communities?

A

outbreaks often occur in closed communities

144
Q

what are the symptoms of norovirus infection?

A

acute gastroenteritis, recovery 1 – 3 days

145
Q

what is the treatment for norovirus infection?

A

not usually required

146
Q

how is norovirus infection diagnosed?

A

sample PCR

147
Q

what are the most common species of Campylobacter?

A

Campylobacter jejuni
Campylobacter coli

148
Q

how is Campylobacter infection transmitted?

A

undercooked meat (especially poultry)

untreated water

unpasteurised milk

149
Q

how dangerous is Campylobacter?

A

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

150
Q

how is Campylobacter treated?

A

not usually required BUT azithromycin can be given (usually resistant to fluoroquinolones otherwise)

151
Q

which antibiotic can be prescribed to treat Campylobacter infection?

A

azithromycin (macrolide)

152
Q

what is the epidemiology of Campylobacter?

A

approx 280,000 cases per year in UK (65,000 confirmed)

commonest cause of food poisoning in the UK

153
Q

what is E.coli?

A

diverse group of gram-negative intestinal bacteria

154
Q

how many pathotypes of E.coli are there?

A

approx six harmful pathotypes but most are harmless

155
Q

name the six pathotypes of E.coli

A

enterotoxigenic E. coli (ETEC)

enteroinvasive E. coli (EIEC)

enterohaemorrhagic or Shiga toxin-producing E. coli (EHEC/STEC)

enteropathogenic E. coli (EPEC)

enteroaggregative E. coli (EAEC)

diffusely adherent E. coli (DAEC)

156
Q

what is enterotoxigenic E.coli and what does it cause?

A

cholera-like toxin

= watery diarrhoea

157
Q

what is enterohaemorrhagic E.coli and what does it cause?

A

E. coli O157 serogroup, Shiga toxin/verotoxin

= approx 5-10% get haemolytic uraemic syndrome (loss of kidney function)

(most problematic pathotype of E.coli)

158
Q

what is enteroinvasive E.coli and what does it cause?

A

Shigella like illness

= bloody diarrhea

159
Q

what is enterohaemorrhagic E. coli also known as?

A

Shiga toxin-producing E.coli

160
Q

which pathotype of E. coli is the most problematic?

A

enterohaemorrhagic or Shiga toxin-producing E. coli (EHEC/STEC)

161
Q

where is Clostridium difficile most common?

A

in a hospital setting in patients currently on antibiotics

162
Q

explain the state of C. diff in the healthy, stable gut

A

few, minimal C. diff microbes (exist normally in healthy gut but in small amounts)

loads of disturbance-sensitive commensals

few information-tolerant commensals

163
Q

explain the state of C. diff in the intermediate, dysbiotic gut

A

more C. diff microbes than normal

fewer disturbance-sensitive commensals

more information-tolerant commensals

164
Q

explain the state of C. diff in the diseased gut

A

very many C. diff microbes than normal

very few disturbance-sensitive commensals

very many information-tolerant commensals

= also increased inflammation-derived metabolites present

165
Q

how is a patient with C. diff managed?

A

isolate patient (very contagious)

stop current antibiotics

start on metronidazole or vancomycin

166
Q

which medication is given to treat C. diff infection?

A

metronidazole or vancomycin

167
Q

what is the recurrence rate of C. diff infection?

A

recurrence rate 15-35% after initial infection

= becomes increasingly difficult to treat

168
Q

how is C. diff infection treated?

A

wither w metronidazole or vancomycin

OR

faecal microbiota transplantation (98% cure rate)

169
Q

which virus is most commonly associated with outbreaks in small, closed communities?

A

norovirus

170
Q

which virus is the most common cause of food poisoning in the UK?

A

campylobacter

171
Q

what causes dysbiosis?

A

exogenous disturbance (e.g. antibiotics)

brs (phase 1b) (71 decks)

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