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gastro yr 2 > immunology of gut > Flashcards

immunology of gut Flashcards

1
Q

what structures is the gut tolerant to and what does it initiate immunoreactivity against

A

tolerant:
food antigens
commensal bacteria

immunoreactive:
pathogens

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2
Q

Sa of Gi tract

A

200 m2

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3
Q

what does the Gi tract have that helps with the immune response

A

huge antigen load (Many antignes in there)

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4
Q

number of bacteria in microbiome

A

10^4

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5
Q

role of microbiome IN GUT - local

and role in body as a whole

A

presents antigens (dietary ect)
first responce to pathogens

immunological homeostasis of gut and development of healthy immune system

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6
Q

what does state of “restrained activation” in gut refer to?

A

dual immunological role of gut
first tolerance to pathogens (just absorbs them)
theeen
active immune response triggered

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7
Q

what kind of animals (mice in this case) are GI immune studies carried out on and why?

A

germ free mice bc they dont have germs so dont have very developed immune responce so have many defects and you can do selective colonisation and grow specific aspects they dont have so you see the effects

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8
Q

what are 2 things that are important that germ free mice have a immunol. defect in and what structure missing causes that?

A

1) DEFECT IN DEVELOPMENT OF SMALL INTESTINE

bc they have FEWER AND LESS CELLULAR PAYERS PATCHES

2) DEFFEctive xpression of angiogenin 4 from paneth cells

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9
Q

explain the concept of the microbiome.

A

microbiome bacteria are more cells than total cells in body - and 100 times our own genes

they carry out essential functions that we have not had to evolve to do ( so they act as like an extension of our own cells/ body)

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10
Q

what is the pattern of numbers of microbiome bacteria along the GI tract and why?

A

increasing numbers as we go down bc of less and less storng digestive enzymes of host produced - colon: none

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11
Q

what are factors that lead to microbiome bacterial growth- increased cell numbers

A

ingested and secreted nutrients

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12
Q

factors that lead to bacterial lysis and bacterial elimination -> decr cell (bact) numbers

A

lysis: caused by: chemical digestive factors

bacterial elimination caused by: peristalsis, contractions, defecation

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13
Q

What is dysbiosis

A

altered microbiota composition - when theres more pathobionts than symbionts

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14
Q

possible causes of dysbiosis

A

inflammation and infection
diet
xenobiotics (substance foreign to animal life- chemmicals- drugs - pollutnats)
hygiene
genetics

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15
Q

specific diseases caused by disrupted microbiome intestinal

A

IBD coeliac disease

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16
Q

systemic diseases caused by dysbiosis

A

t1d
atherosclerosis (TMAO: artery wall deposits)
RA
cancers (SCAFS (short chain fatty acids- toxins that cause it)

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17
Q

BRAIN disease from dysbiosis

A

stress
autism ( EPS 4- toxin released that causes)
MS

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18
Q

liver disease dysbiosis

A

NAFLD
NASH

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19
Q

ADIpose tissue disease for dysbiosis

A

obesity
metabolic disease

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20
Q
A
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20
Q

what is the first line of mucosal defence against intruding pathogens

A

1) PHYSICAL barriers : first line: anatomical:
a) peristalsis and b) epithelial barrier
chemical: a) enzymes b) acid ph

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21
Q

second line defence in mucosa against pathogens

A

commensal bacteria

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22
Q

second line defence against bact

A

MALT and galt

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23
Q

epithelial barrier structure?

A

basically crypts of lieberkuhn:
1) at their base its the paneth cells doing the secretions (antimicrobial peptides- defensins and lysozyme)

above its the epithelial monolayer with tight junctions

surface its goblet cells : mucus layer

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24
Q

what does malt stand for

A

mucosa associated lympoid tissue

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25
Q

where is malt found (in tissue layers terms and highest prevalence in body part terms)

A

below epithelium in submucosa layer

oral cavity rich in immunological tissue- first thymal defence in mouth

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26
Q

what is MALT structurally

A

lymphoid mass containing lymphoid follicles.

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

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27
Q

what does galt stand for and what is it responsible for

A

gut associated lymphoid tissue Responsible for both adaptive & innate immune responses through generations of lymphoid cells & Abs

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28
Q

non- organised GALTs

A

Intra-epithelial lymphocytes
Make up 1/5th of intestinal epithelium, e.g. T-cells, NK cells

Lamina propria lymphocytes

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29
Q

organised GALTs and where along gI theyre found + any other relevant feature

A

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

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30
Q

what are the differences in small and large intestine in terms of GALTS and why

A

so dependng on function theres differences in galts:
small int: mor eabsorption more SA, more microbiota, more ORGANISED galts

large: less microbiota bc less absorption also less SA so less ORGANISED GALTS but MORE PREVALENT: UNORGANISED GALTS - IgA more prev than small!!

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31
Q

where do immune cells -T-cells, IgA B cells, macrophages and DCs normally sit in vili of small and large intestine?

A

sit in the lamina propria

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32
Q

what is the lamina propria?

A

its connective tissue- no cells in it

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33
Q

Where are payers patches found in GI tract and in depth of the tissue layers?

A

in submucosa layer mainly in distal ileum

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34
Q

what are payers patches composed of?

A

aggregated lymphoid follicles covered with follicle associated epithelium (FAE)
+
its an organised collection of naive t cells and b cells

35
Q

what features/ elements does FAE lack compared to other GI epithelium?

A

lacks goblet cells, secretory IgA, microvilli

36
Q

what is a requirement for the development of payers patches?

A

exposure to bacterial microbiota

37
Q

how many payers patches are there in a last trimester foetus and teens

A

50 in last trimester foetus and 250 in teens

38
Q

what is an M cell and what is its function (also what does it stand for)

A

a cell type that sits within FAE- stands for microfold

mcells:
1) uptake antigens
1) express igA receptors fascilitating transport of IgA bacteria complexes into peyers patches

39
Q

in the electron microscopic image what is the fluffy protrusion and what is the dip? (slide 13)

A

microvilli- protrusion
dip: m cells

40
Q

what is an alternative route of antigen uptake (Alternative to m cell antigen detection)? when does this happen?

A

trans epithelial dendritic cell antigen detection, the dendritic cell squeezes through the tight junction of the mucosal epithelium and captures and antigen, then goes straigh back to mesenteric lymph node

this happens when theres an increased antigen loead (m cell no enough)

41
Q

what Ig class do mature naive B cells initially express in Payers patches? what changes on antigen presentation?

A

IgM- class swithes to IgA

42
Q

what cells influence b- cell maturation?

A

T cells and epithelial cells influence b cell mat through cytokine production

43
Q

what happens to b cells when they mature

A

they turn into Iga secreting plasma cells

44
Q

what part of the villi do mature b cells “populate”?

A

lamina porpria

45
Q

do all gut b cells secrete IgA?

A

up to 90% do

46
Q

what are the two types of circulating IgA and what situation is each designated for

A

Iga bound on t and b cells and secretory IgA: secreted by bcells towards late stage of infection/infl responce.

47
Q

how does secretory IgA work?

A

binds luminal antigen and prevents its adhesion on epithelial cell and thus its invasion

48
Q

there is an”immediate” and a more “delayed” immune responce in gut immune system. what is the early and what i the delayed?

A

the immediate is the one with the Iga and b cells ect

the delayed is the “lymphocyte homing and circulation process.”

49
Q

what happens in “lymphocyte homing and circulation”

A

1) antigens in the lumen are presented to the payers patches and they get activated

2) they go to mesenteric lymph nodes where lymphocyte proliferation happens

3) they travel to thoracic duct, to circulation may go to skin,tonsils, balt,and then back to lamina propria in villi ( circulation pricess)

this builds immunity over weeks- long lasting immune responce

50
Q

diving more detail into the homing process of T-cells what is the process? what particles involved are important?

A

homing is the process of the naive t cells getting into payers patches.

homingcascade:
t cell starts form High Endothelial Venule (HEV) and it goes thorugh
1) rolling
2) activation by binding of a4b7 integrin on t cell with MAdCAM-1 on tihgh junction - this interaction allows t cell to go through tight junction

3) ARREST: the going through is called that

51
Q

what is the life span of enterocytes and goblet cells and what is that of other epithelial cell types?

A

about 36 hrs for enterocyte and goblet vs weeks/months for other epithelial cells

52
Q

why do enterocytes and goblet cells have such short life span?

A

1) enterocytes are first line of defence against GI pathogens AND can be directly affected by toxic substances in diet

2) this way the effects of agents (ex xenobiotics ect) which may interfere with cell function, metabolic rate ect will be diminished

3) any lesions are short lived

4) if the escalator like transit (process of new enterocytes “escalating” from depth of crypts to replace old at top)
is interupted through imparied production of new cells (radiation) severe intestinal dysfunction would occur.

53
Q

what kind of pathogen in cholera and what is the name of the pathogens causing cholera infection?

A

acute bacterial disease

caused by vibrio cholerae serogroups O1+O139

54
Q

through what mechanism does vibrio cholerae infect ?

A

bacteria reach small intestine
-> contact with epithelium and releases cholera enterotoxin

55
Q

transmission route of cholera

A

faecal-oral route through contaminated water and food

56
Q

main and other symptoms of cholera

A

main: watery diarrhoea and severe dehydration
other: nausea, vomiting and abdo pain

57
Q

how is cholera diagnosed- 2ways -1 golden standard

A

gold standard: bacterial culture from stool sample on selective agar

rapid dipstick tests are also available

58
Q

treatment of cholera

A

oral rehydration - 80% of cases can be successfully treated

59
Q

what is the only actual medicine involving intervention for cholera?

A

vaccine - dukoral: oral, activated

60
Q

what is cholera distribution in the world rn?

A

uk not that common: 1893-2017 13 cases
globallly 1.3-4 million cases average 95,000 deaths annually

61
Q

what are some Viral differentials for diarrhoea? who/when do they attack?

A

rotavirus (children) , norovirus (winter vomiting bug)

62
Q

protozoal causes of diarrhoea

A

giardia lamblia
entamoeba histolytica

63
Q

bacterial causes of diarrhoea other than cholera

A

Campylobacter jejuni
Escherichia coli
Salmonella
Shigella
Clostridium difficile

64
Q

what type of virus is rotavirus (DNA or RNA) and where does it replicate + how many subtypes are there? which more common in humans?

A

RNA virus,
replicates in enterocytes
A-E 5types- A most common

65
Q

what is the most common cause of diarrhoea in infants and young children worldwide

A

rotaviruses

66
Q

treatment of rotaviruses - what is it- how effective is it- what development changed the number of kids infected

A

Oral rehydration therapy
Still causes ~ 200,000 deaths/year.
Before vaccine, most individuals had an infection by age 5-

67
Q

do repeated infections with rotavirus develop immunity?

A

yes

68
Q

details of vaccine for rotavirus:

A

Live attenuated oral vaccine (Rotarix)

against type A

introduced in UK July 2013.

69
Q

distinction between norovirus and norwalk virus

A

genus vs species in that order

70
Q

norovirus: rna or dna and incubation period?

A

rna
24-48 hrs

71
Q

transmission of norovirus - route and how long do you transmit for - (typical transmission story?)

A

Faecal-oral transmission.
Individuals may shed infectious virus for up to 2 weeks (even after recovery which takes 1-2 days)
Outbreaks often occur in closed communities (ex. Cruise)

72
Q

symptoms of norovirus and recovery and diagnosis?

A

acute gastroenteritis recovery 1-3 days

sample PCR

73
Q

epidemiology of norovirus?

A

estimated 685 million cases and 200,000 deaths/ year

74
Q

is cholera, norovirusor notavirus more common and deadly nowadays ?

A

noroviruses and notavirus equally more deadly than cholera and also more prevalent.

75
Q

what is the most common cause of food poisoning in uk?

A

campylobacter

Estimated 280,000 cases per year in UK, 65,000 confirmed

76
Q

most common speies of campylobacter (kabili- curved bacteria lol)

A

Campylobacter jejuni, Campylobacter coli

77
Q

usual way of transmission of campylobacter. does thereneedto be high or low bacteria number to cause infection?

A

Undercooked meat (especially poultry), untreated water & unpasteurised milk
Low infective dose, a few bacteria (<500) can cause illness

77
Q

treatment for capylobacter infection

A

Not usually required
Azithromycin (macrolide) is standard antibiotic
Resistance to fluoroquinolones is problematic

78
Q

what gram bacteria is e coli and where does it infect? how harmful compared to others?
are all e colis associated with diarrhoea?

A

diverse group of gram- negative intestinal bacteria

most harmless

not all assoc with diarr

79
Q

how many and which pathotypes of ecoli are associated

A

6 pathotypes
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)

80
Q

describe Enterotoxigenic E. coli (ETEC) infection

A

Cholera like toxin
Watery diarrhoea

81
Q

describe Enterohaemorrhagic or Shiga toxin-producing E. coli (EHEC/STEC) infection

A

E. coli O157 serogroup, Shigatoxin/verotoxin
5-10% get haemolytic uraemic syndrome: loss of kidney function

82
Q

describe Enteroinvasive E. coli (EIEC) infection

A

Shigella like illness
Bloody diarrhea

83
Q

how does c diff infect organism

A

1) exogenous disturbance such as anitbiotic leads to dysbiosis - intermediate dysbiotic stage- leads to pathogen induced disturbance - diseasedstate

84
Q

why is c diff highly infectious?

A

bc it survives on surfaces

85
Q

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. (bc very antibiotic resistant)
Faecal Microbiota Transplantation (FMT) – 98% cure rate

gastro yr 2 (9 decks)

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