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

Gastro - Gut Immunology Flashcards

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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
What are AHR ligands? What are their effects?
→ Aryl hydrocarbon receptor ligands → associated with MS + RA
26
How does dysbiosis affect the brain?
→ stress → autism → MS
27
How does dysbiosis affect the lungs?
→ Asthma
28
How does dysbiosis affect the liver?
→ NAFLD (Nonalcoholic fatty liver disease) → NASH (Non-Alcoholic SteatoHepatitis)
29
How does dysbiosis affect the adipose tissue?
→ obesity → metabolic disease
30
How does dysbiosis affect the intestines?
→ IBD → Coeliac disease
31
How does dysbiosis cause systemic diseases?
pathogens create bacterial metabolites + toxins e.g. TMAO, 4-EPS, SCFSAs, bile acids, AHR ligands) which can adversely affect the body
32
What are the different categories of ways in which the body defends against bacteria?
→ physical (anatomical) → physical (chemical) → commensal bacteria → immunological
33
How does the body defend itself anatomically?
→ epithelial barrier → mucosal defense → peristalsis
34
How does the body defend itself chemically?
→ enzymes → acidic pH
35
How does the epithelial barrier help defend the body?
→ mucus layer produced by goblet cells → epithelial mono-layer + tight junctions → paneth cells in small intestine
36
How do Paneth cells defend the body?
→ living in the bases of crypts of Lieberkühn → secrete antimicrobial peptides (defensives) + lysosomes
37
How do commensal bacteria defend the body?
occupy an ecological nice and act as an ecological barrier
38
What is the third line of defense?
immunological → MALT (mucosa associated lymphoid tissue) → GALT (gut associated lymphoid tissue)
39
\*What is MALT? Where is it found?
→ mucosa associated lymphoid tissue → found in the submucosa below the epithelium, as lymphoid mass containing lymphoid follicles
40
How does MALT help defend the body?
→ 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
What is GALT?
→ 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
What are the 2 categories of GALT?
→ non-organised → organised
43
\*What is the non-organised component of GALT?
→ Intra-epithelial lymphocytes (Make up 1/5th of intestinal epithelium, e.g. T-cells, NK cells) → Lamina propria lymphocytes
44
What is organised GALT?
→ Peyer’s patches (small intestine) → Caecal patches (large intestine) → Isolated lymphoid follicles → Mesenteric lymph nodes (encapsulated)
45
What are Peyer's patches? Where are they found?
→ immune sensors → Found in submucosa small intestine – mainly distal ileum
46
What is the structure of Peyer's Patches? What do they contain?
→ 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
How do Peyer's patches develop?
development. requires exposure to bacterium micro bacterial
48
How do Peyer's patches take up antigens?
→ 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
What is an alternative way for Peyer's patches to pick up antigens?
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
What is the B-cell response in Peyer's patches?
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
How are secretory IgAs formed + released?
52
How much of the gut's B-cells can secrete IgAs?
90%
53
What is the purpose of the secretory IgAs?
→ binds to luminal antigen → prevents the pathogen adhesion + consequent invasions
54
What is the process of lymphocyte homing + circulation?
v
55
What is a BALT?
bronchus associated lymphoid tissue
56
How do lymphocytes undergo the process of gut homing + return to circulation?
57
What is the average turnover of enterocytes + goblet cells of the small intestine?
about 36 hours, compared to weeks/months for other epithelial cell types
58
Why is the turnover for small intestine cells so short?
→ 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
\*What is the mechanism of cholera infection?
→ 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
How is cholera transmitted?
→ Transmitted through faecal-oral route → Spreads via contaminated water & food
61
What are the main symptoms of cholera?
→ Severe dehydration → watery diarrhoea → Vomiting → nausea → abdominal pain.
62
How is cholera infection diagnosed?
bacterial culture from stool sample on selective agar is the gold standard, rapid dipstick tests also available.
63
How is cholera infection treated?
→ oral-rehydration is the main management → up to 80% of cases can be successfully treated
64
What is the vaccine for cholera?
Dukoral, oral, inactivated
65
What can cause infectious diarrhoea virally?
→ Rotavirus (children) → Norovirus “winter vomiting bug”
66
What can cause bacterial infectious diarrhoea?
→ Campylobacter jejuni → Escherichia coli → Salmonella → Shigella → Clostridium difficile
67
What can causes infectious diarrhoea parasitically?
→ Giardia lamblia → Entamoeba histolytica
68
What is rotavirus? What are the different types?
→ RNA virus, replicates in enterocytes. → 5 types, A – E → type A most common in human infections
69
What is the epidemiology of rotavirus?
→ Most common cause of diarrhoea in infants & young children worldwide → Still causes ~ 200,000 deaths/year
70
What is the treatment for rotavirus?
→ Oral rehydration therapy → Before vaccine, most individuals had an infection by age 5 → repeated infections develop immunity
71
Does rotavirus have a vaccine?
Live attenuated oral vaccine (Rotarix) against type A introduced in UK July 2013
72
What is norovirus?
RNA virus Incubation period 24-48 hours
73
What is the transmission of norovirus?
Faecal-oral transmission. Individuals may shed infectious virus for up to 2 weeks Outbreaks often occur in closed communities
74
What are the symptoms of norovirus infection?
Acute gastroenteritis, recovery 1 – 3 days
75
What is the treatment of norovirus?
Not usually required
76
How is norovirus infection diagnosed?
Sample PCR.
77
How is rotavirus transmitted?
faecal-oral route
78
What is campylobacter? What does it cause?
"curved bacteria", causes food poisoning
79
What are the common species?
→ campylobacter jejuni → campylobacter coli
80
How is campylobacter transmitted?
→ Undercooked meat (especially poultry), untreated water & unpasteurised milk → Low infective dose, a few bacteria (\<500) can cause illness
81
What is the treatment for campylobacter infection?
→ Not usually required → Azithromycin (macrolide) is standard antibiotic
82
What is a problem in campylobacter treatment?
Resistance to fluoroquinolones is problematic
83
What is the epidemiology of campylobacter infections?
→ Estimated 280,000 cases per year in UK, 65,000 confirmed → Commonest cause of food poisoning in the UK
84
What is E.coli?
→ Escherichia coli → Diverse group of Gram-negative intestinal bacteria → Most harmless → 6 ”pathotypes” associated with diarrhoea (diarrhoeagenic):
85
What are the 6 types of diarrhoeagenic E.coli?
→ 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
What are the symptoms of enterotoxigenic E.coli?
→ cholera like toxin → watery diarrhoea
87
What are the symptoms of enteroinvasive E.coli?
→ shigella like illness → bloody illness
88
What are the symptoms of Enterohaemorrhagic or Shiga toxin-producing E. coli?
→ E. coli O157 serogroup, Shigatoxin/verotoxin → 5-10% get haemolytic uraemic syndrome: loss of kidney function
89
How does C.Diff infect + disturb gut?
v
90
How is C.Diff infection treated?
→ Isolate patient (very contagious) → Stop current antibiotics → Metronidazole, Vancomycin → Faecal Microbiota Transplantation (FMT) – 98% cure rate
91
What is one of the biggest causes of C.Diff?
antibiotic over-use or incorrect use
92
What is the recurrence rate of C.Diff infection?
Recurrence rate 15-35% after initial infection, increasingly difficult to treat.

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

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