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!!!!! BRS YR2 !!!!! > Gastro - Gut Immunology > Flashcards

Gastro - Gut Immunology Flashcards

1
Q

What is the surface area of the GI tract?

A

200m^2

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2
Q

What part of the body has the most complex + diverse immune system?

A

GI tract

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3
Q

What is the GI tract exposed to 24/7?

A

massive antigen load

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4
Q

What is a part of the massive antigen load the GI tract is exposed to?

A

→ Resident microbiota 1014 bacteria
→ Dietary antigens
→ Exposure to pathogens

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5
Q

What kind of state does the GI tract’s immune system have to be in?

A

State of “restrained activation”
– Tolerance vs active immune response
– Dual immunological role

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6
Q

What does the GI tract have to have tolerance for?

A

→ food antigens
→ commensal bacteria

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7
Q

What does the GI tract have to have immunoreactivity for?

A

pathogens

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8
Q

Why is the presence of bacterial microbiota important in the GI tract?

A

Immune homeostasis of gut & development of healthy immune system requires presence of bacterial microbiota.

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9
Q

How do you explore the relationship between microbiota + immune system?

A

using gnotobiotic organisms:
→ germ free organisms that they introduce particular germs to and then compare with conventional house mice
→ can help you identify immunological defects in gnotobiotic organisms

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10
Q

How much gut bacteria do we have?

A

10^14 compared to 10^13 cells in the body
→ most densely populated ecosystem on Earth

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11
Q

What are the main types of bacteria found?

A

4 major phyla:
→ bacteroidetes
→ firmicutes
→ actinobacteria
→ proteobacteria

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12
Q

What are the genetic benefits of having gut flora?

A

Provide traits we have not had to evolve on our own - Genes in gut flora 100 times our own genome.

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13
Q

What promotes bacterial growth in the GI? Why?

A

→ ingested nutrients
→ secreted nutrients

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14
Q

What reduces bacterial growth in the GI? Why?

A

→ chemical digestive factors –> leads to bacterial lysis
→ peristalsis, contractions, defecations –> leads to bacterial elimination

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15
Q

What is the bacterial content of the different parts of the GI tract? Why?

A
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16
Q

What is dysbiosis?

A

altered microbiota composition
→ when there is an imbalance between symbionts and pathobionts
→ higher proportion of pathobionts will cause inflammation

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17
Q

What is a symbiont?

A

has no benefits or harm to the host

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18
Q

What is a commensal?

A

benefits from association with the host but has no effect on the host

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19
Q

What is a pathobiont?

A

usually a symbiont, but can cause harm when dysregulated

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20
Q

What factors can cause dysbiosis?

A

→ infection or inflammation
→ diet
→ xeno biotics
→ hygiene
→ genetics

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21
Q

What does dysbiosis cause?

A

Type 1 Diabetes Rheumatoid Arthritis Atherosclerosis

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22
Q

What is TMAO? What are its effects on the body?

A

→ Trimethylamine Oxide
→ increases cholesterol deposition in the artery walls
→ increases chances of atherosclerosis

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23
Q

What is 4-EPS? What are its effects?

A

→ 4-ethylphenyl sulphate
→ associated with autism

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24
Q

What is SCFAs? What are their effects?

A

→ short chain fatty acids
→ decreased numbers are associated with IBD
→ increased numbers are associated with neuropsychiatric disorders, e.g. stress

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25
Q

What are AHR ligands? What are their effects?

A

→ Aryl hydrocarbon receptor ligands
→ associated with MS + RA

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26
Q

How does dysbiosis affect the brain?

A

→ stress
→ autism
→ MS

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27
Q

How does dysbiosis affect the lungs?

A

→ Asthma

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28
Q

How does dysbiosis affect the liver?

A

→ NAFLD (Nonalcoholic fatty liver disease)
→ NASH (Non-Alcoholic SteatoHepatitis)

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29
Q

How does dysbiosis affect the adipose tissue?

A

→ obesity
→ metabolic disease

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30
Q

How does dysbiosis affect the intestines?

A

→ IBD
→ Coeliac disease

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31
Q

How does dysbiosis cause systemic diseases?

A

pathogens create bacterial metabolites + toxins
e.g. TMAO, 4-EPS, SCFSAs, bile acids, AHR ligands) which can adversely affect the body

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32
Q

What are the different categories of ways in which the body defends against bacteria?

A

→ physical (anatomical)
→ physical (chemical)
→ commensal bacteria
→ immunological

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33
Q

How does the body defend itself anatomically?

A

→ epithelial barrier
→ mucosal defense
→ peristalsis

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34
Q

How does the body defend itself chemically?

A

→ enzymes
→ acidic pH

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35
Q

How does the epithelial barrier help defend the body?

A

→ mucus layer produced by goblet cells
→ epithelial mono-layer + tight junctions
→ paneth cells in small intestine

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36
Q

How do Paneth cells defend the body?

A

→ living in the bases of crypts of Lieberkühn
→ secrete antimicrobial peptides (defensives)
+ lysosomes

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37
Q

How do commensal bacteria defend the body?

A

occupy an ecological nice and act as an ecological barrier

38
Q

What is the third line of defense?

A

immunological
→ MALT (mucosa associated lymphoid tissue)
→ GALT (gut associated lymphoid tissue)

39
Q

*What is MALT? Where is it found?

A

→ mucosa associated lymphoid tissue
→ found in the submucosa below the epithelium, as lymphoid mass containing lymphoid follicles

40
Q

How does MALT help defend the body?

A

→ lots of lymphoid mass containing lymphoid follicles
→ Follicles are surrounded by HEV (high endothelial venules) postcapillary venules, allowing easy passage of lymphocytes
→ oral cavity is rich in immunological tissue

41
Q

What is GALT?

A

→ gut associated lymphoid tissue
→ Responsible for both adaptive & innate immune responses
→ Consists of B & T lymphocytes, macrophages, APC (dendritic cells), and specific epithelial & intra-epithelial lymphocytes

42
Q

What are the 2 categories of GALT?

A

→ non-organised
→ organised

43
Q

*What is the non-organised component of GALT?

A

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

44
Q

What is organised GALT?

A

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

45
Q

What are Peyer’s patches? Where are they found?

A

→ immune sensors
→ Found in submucosa small intestine – mainly distal ileum

46
Q

What is the structure of Peyer’s Patches? What do they contain?

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
→ sub-epithelial dome contains dendritic cells

47
Q

How do Peyer’s patches develop?

A

development. requires exposure to bacterium micro bacterial

48
Q

How do Peyer’s patches take up antigens?

A

→ Antigen uptake via M (microfold) cells within FAE
→ M cells express IgA receptors, facilitating transfer of IgA-bacteria complex into the Peyer’s patches

49
Q

What is an alternative way for Peyer’s patches to pick up antigens?

A

antigen sampling through trans-epithelial dendritic cells:
→ dendritic cells from mesenteric lymph nodes send dendrites through tight junctions to collect antigens + bring them back

50
Q

What is the B-cell response in Peyer’s patches?

A

B-cell adaptive response:
→ 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

51
Q

How are secretory IgAs formed + released?

A
52
Q

How much of the gut’s B-cells can secrete IgAs?

A

90%

53
Q

What is the purpose of the secretory IgAs?

A

→ binds to luminal antigen
→ prevents the pathogen adhesion + consequent invasions

54
Q

What is the process of lymphocyte homing + circulation?

A

v

55
Q

What is a BALT?

A

bronchus associated lymphoid tissue

56
Q

How do lymphocytes undergo the process of gut homing + return to circulation?

A
57
Q

What is the average turnover of enterocytes + goblet cells of the small intestine?

A

about 36 hours, compared to weeks/months for other epithelial cell types

58
Q

Why is the turnover for small intestine cells so short?

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.

59
Q

*What is the mechanism of cholera infection?

A

→ acute bacterial disease caused by Vibrio cholerae serogroups O1 & O139
→ Bacteria reaches small intestine
→ contact with epithelium & releases cholera enterotoxin.
→ taken in + increases aneylate cyclase activity
→ increases cAMP
→ causes active secretion of salts, bicarbonates, etc.
→ water follows
→ causes diarrhoea

60
Q

How is cholera transmitted?

A

→ Transmitted through faecal-oral route
→ Spreads via contaminated water & food

61
Q

What are the main symptoms of cholera?

A

→ Severe dehydration
→ watery diarrhoea
→ Vomiting
→ nausea
→ abdominal pain.

62
Q

How is cholera infection diagnosed?

A

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

63
Q

How is cholera infection treated?

A

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

64
Q

What is the vaccine for cholera?

A

Dukoral, oral, inactivated

65
Q

What can cause infectious diarrhoea virally?

A

→ Rotavirus (children)
→ Norovirus “winter vomiting bug”

66
Q

What can cause bacterial infectious diarrhoea?

A

→ Campylobacter jejuni
→ Escherichia coli
→ Salmonella
→ Shigella
→ Clostridium difficile

67
Q

What can causes infectious diarrhoea parasitically?

A

→ Giardia lamblia
→ Entamoeba histolytica

68
Q

What is rotavirus? What are the different types?

A

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

69
Q

What is the epidemiology of rotavirus?

A

→ Most common cause of diarrhoea in infants & young children worldwide
→ Still causes ~ 200,000 deaths/year

70
Q

What is the treatment for rotavirus?

A

→ Oral rehydration therapy
→ Before vaccine, most individuals had an infection by age 5
→ repeated infections develop immunity

71
Q

Does rotavirus have a vaccine?

A

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

72
Q

What is norovirus?

A

RNA virus
Incubation period 24-48 hours

73
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

74
Q

What are the symptoms of norovirus infection?

A

Acute gastroenteritis, recovery 1 – 3 days

75
Q

What is the treatment of norovirus?

A

Not usually required

76
Q

How is norovirus infection diagnosed?

A

Sample PCR.

77
Q

How is rotavirus transmitted?

A

faecal-oral route

78
Q

What is campylobacter? What does it cause?

A

“curved bacteria”, causes food poisoning

79
Q

What are the common species?

A

→ campylobacter jejuni
→ campylobacter coli

80
Q

How is campylobacter transmitted?

A

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

81
Q

What is the treatment for campylobacter infection?

A

→ Not usually required
→ Azithromycin (macrolide) is standard antibiotic

82
Q

What is a problem in campylobacter treatment?

A

Resistance to fluoroquinolones is problematic

83
Q

What is the epidemiology of campylobacter infections?

A

→ Estimated 280,000 cases per year in UK, 65,000 confirmed
→ Commonest cause of food poisoning in the UK

84
Q

What is E.coli?

A

→ Escherichia coli
→ Diverse group of Gram-negative intestinal bacteria
→ Most harmless
→ 6 ”pathotypes” associated with diarrhoea (diarrhoeagenic):

85
Q

What are the 6 types of diarrhoeagenic 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)

86
Q

What are the symptoms of enterotoxigenic E.coli?

A

→ cholera like toxin
→ watery diarrhoea

87
Q

What are the symptoms of enteroinvasive E.coli?

A

→ shigella like illness
→ bloody illness

88
Q

What are the symptoms of Enterohaemorrhagic or Shiga toxin-producing E. coli?

A

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

89
Q

How does C.Diff infect + disturb gut?

A

v

90
Q

How is C.Diff infection treated?

A

→ Isolate patient (very contagious)
→ Stop current antibiotics
→ Metronidazole, Vancomycin
→ Faecal Microbiota Transplantation (FMT) – 98% cure rate

91
Q

What is one of the biggest causes of C.Diff?

A

antibiotic over-use or incorrect use

92
Q

What is the recurrence rate of C.Diff infection?

A

Recurrence rate 15-35% after initial infection, increasingly difficult to treat.

!!!!! BRS YR2 !!!!! (72 decks)

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