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BRS Year 2 > GI immunology of the gut > Flashcards

GI immunology of the gut Flashcards

1
Q

What makes up the massive antigen load of the gut? (3)

A
  • resident microbiota
  • dietary antigens
  • exposure to pathogens
  • must balance tolerance and active immune response- “restrained activation”
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2
Q

What makes up the gut microbiota?

A

4 major phyla of bateria (bacteroidetes, firmcutes, actinobacteria, proteobacteria)

  • viruses
  • fungi
  • -> provide traits that we didn’t have to evolve on our own: genes in gut flora 100 times our own genome
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3
Q

benefits of gut microbiota (4)

A
  • provide essential nutrients that we can’t manufacture
  • metabolise indigestible compounds
  • defence against colonisation opportunistic pathogens
  • contribute to intestinal architecture
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4
Q

why is the microbiome of the stomach relatively small?

A

its acidic pH

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5
Q

why is the microbiome of the liver relatively small?

A

bile acids

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6
Q

what is found in the pancreas that affects the microbiome? (3)

A

trypsin
amylase
carboxypeptidase

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7
Q

what is found in the small intestine that affects the microbiome?

A
  • brush border

- enzymes

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8
Q

what is found in the colon that affects the microbiome?

A

no host digestive factors

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9
Q

three relationships that the gut flora have with the body

A
  • symbiotic
  • commensal
  • pathobiont (symbionts that can cause inflammation and disease)
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10
Q

what is a commensal relationship

A
  • no benefit but no harm to host
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11
Q

what do symbionts contribute to?

A

regulation of the gut

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12
Q

what do pathobionts contribute to?

A

inflammation

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13
Q

what can affect whether a relationship is healthy or dysbiotic? (5)

A
  • infection/inflammation
  • diet
  • xenobiotics
  • hygiene
  • genetics
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14
Q

examples of bacterial metabolites and toxins in dysbiosis (5)

A

TMAO - associated with atherosclerosis
4-EPS- associated with autism
SCFAs- low number associated w/ IBD, high number w/ stress
bile acids
AHR ligand- associated w/ MS, rheumatoid arthritis and asthma

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15
Q

what are the physical gut barriers? (Anatomical (2), chemical (2))

A 
Anatomical:
- epithelial barrier
- peristalsis
Chemical:
- enzymes
- acidic pH
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16
Q

defensive features of the epithelial barrier (3)

A
  • mucus layer (goblet cells)
  • epithelial monolayer (tight junctions)
  • Paneth cells in the base of crypts of lieberkuhn and secrete antimicrobial defensins and lysozyme
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17
Q

how are commensal bacteria useful for defense?

A
  • occupy ecological niche

second line of defense

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18
Q

two immunological defenses following invasion

A
  • mucosa associated lymphoid tissue (MALT)
  • gut associated lymphoid tissue (GALT)
    3rd line of defence
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19
Q

where are MALT found?

A
  • in submucosa below the epithelium, as lymphoid mass containing lymphoid follicles
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20
Q

What surrounds MALT?

A

HEV (postcapillary venules) - allows easy passage of lymphocytes

High endothelial venules (HEV) are specialized post-capillary venous swellings characterized by plump endothelial cells as opposed to the usual thinner endothelial cells found in regular venules. HEVs enable lymphocytes circulating in the blood to directly enter a lymph node (by crossing through the HEV).

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21
Q

In which cavity is lots of MALT found?

A
  • the oral cavity

- particularly the palatine, pharyngeal and lingual tonsils

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22
Q

What is GALT responsible for?

A

both adaptive and innate immune responses

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23
Q

What is the largest mass of lymphoid in the body?

A

GALT

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24
Q

what does GALT consist of? (4)

A

B + T lymphocytes
macrophages
APC
specific epithelial + intraepithelial lymphocytes

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25
Q

examples of non-organised GALT tissue (2)

A
  1. intraepithelial lymphocytes - make up 1/5th of intestinal epithelium e.g. T cells and NK cells
  2. lamina propria lymphocytes
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26
Q

examples of organised GALT tissue (4)

A
  1. peyers patches (SI)
  2. caecal patches (SI)
  3. isolated lymphoid follicles
  4. mesenteric lymph nodes (encapsulated)
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27
Q

features of non-organised GALTs

A
  1. stem cells produce enterocytes and paneth cells
  2. eneterocytes migrate to apex of microvili
  3. apoptotic intra-epithelial cells
  4. at base, goblet cells form and go to microvili and produce mucous
  5. paneth cells produce antimicrobial peptides
  6. intraepithelial lymphocytes
  7. laminapropria - majority of intestinal wall immune cells here
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28
Q

How does the large intestines compare to the small intestines

A
  • no villi
  • lots goblet cells
  • no peyer’s patches
29
Q

where are peyer’s patches found?

A

the submucosa of the small intestine - mainly the distal ileum

30
Q

what are peyers patches made of?

A
  • aggregated lymphoid follicles covered with follicle associated epithelium (FAE)
31
Q

features of FAE

A
  • no goblet cells
  • no secretory IgA
  • no microvilli
  • organised collection of naive T and B cells
32
Q

what do peyers patches lie beneath

A

M cells

33
Q

what are M cells for?

A

antigen uptake within FAE
- they express IgA receptors, facilitating transfer of IgA-bacteria complex into the Peyer’s patches

M cells are specialized epithelial cells of the mucosa-associated lymphoid tissues. A characteristic of M cells is that they transport antigens from the lumen to cells of the immune system, thereby initiating an immune response or tolerance.

34
Q

alternative route for antigen transport independent of m cells

A
  • trans-epithelial dendritic cells

- open tight junctions of epithelium and sample bacteria -> transport back to mesenteric lymph nodes

35
Q

What cells do M/dendritic cells activate when they are activated by a pathogen?

A

B cells in peyers patches so that they become IgA-secreting plasma cells

MHCII molecules of dendritic cells migrate to peyers patch -> APC and B and T cells activated and replicated

  • B cells express IgM in Peyer’s patches; on presentation class switches to IgA (more matured)
  • > further maturation into IgA secreting plasma cells
  • populate lamina propria
36
Q

what is the funciton of secretory IgA

A

binds luminal antigen. preventing its adhesions and consequent invasion

37
Q

how are lymphocytes circulated?

A

via the thoracic duct (from mesenteric lymph nodes)

  • from there, enter circulation
  • can then enter peripheral immune system (tonsils, skin, BALT)
38
Q

what is BALT?

A

bronchus associated lymphoid tissue

39
Q

what tether lymphocytes to HEV?

A

MadCAM1: once this happens, activation and rolling arrests.

migrate back to lamina propria

40
Q

enterocytes and goblet cells of the small bowel have a short life span (36 hours)

  • rapid turnover contrasts with lifespan of week/months for other epithelial cells types e.g. lung, blood vessels
  • why>?
A
  • enterocytes are first line of defense against GI pathogens -> first to be affected by toxic substances/pathogens
  • effects of agents which interfere with cells function, metabolic rate etc diminished
  • any lesions are short-lived
41
Q

what causes cholera?

A

vibrio cholerae serogroups O1 and O139

- bacteria reaches small intestine -> contact with epithelium release cholera enterotoxin

42
Q

how is cholera transmitted?

A

faecal-oral route

contaminated food/water

43
Q

main symptoms of cholera

A

severe dehydration + watery diarrhoea

44
Q

other symptoms of cholera

A
  • vomiting
  • nausea
  • abdo pain
45
Q

diagnosis of cholera?

A

becterial culture from stool sample on selective agar = gold standard
-> rapid dipstick tests also available

46
Q

treatment of cholera?

A
  • oral rehydraion is the main management: 80% of cases can be successfully trerated
47
Q

cholera cure?

A

vaccine

dukoral, oral inactivated

48
Q

viral causes of infection diarrhoea?

A 
rotaviru s(kids)
norovirus (winter vom bug)
49
Q

protozoal parasitic causes of infectious diarrhoea?

A

Giardia lamblia

Entamoeba histolytica

50
Q

bacterial causes of infectious diarrhoea? (5)

A 
Campylobacter jejuni
Escheria coli
Salmonella
Shigella
Clostridum difficile
51
Q 
Rotavirus description 
(type, where proliferates, how many types are there)
A

RNA virus
replicates in enterocytes
5 types A-E: A most common in human infections

52
Q

Rotavirus epidemiology

A

Most common cause of diarrhoea in infants and young kids worldwide

53
Q

treatment of rotavirus

A

oral rehydration therapy

54
Q

vaccination type for rotavirus?

A

live attenuated oral vaccine against type A

55
Q

Norovirus/ Norwalk virus description (type. incubation period)

A

RNA virus with incubation period 24-48 hours

56
Q

Norovirus Norwalk virus transmisison

A

facael oral

  • infected may shed infectious virus for up to 2 weeks
  • outbreaks often occur in closed communities
57
Q

Norovirus Norwalk virus symptoms

A

acute gastroenteritis

- recovery 1-3 days

58
Q

Norovirus Norwalk virus treatment

A

not usually required

59
Q

Norovirus Norwalk virus diagnosis

A

sample PCR

60
Q

commonest campylobacter species

A

jejuni and coli

61
Q

campylobacter transmission (3)

A

undercooked meat
unpasteurised milk
low infective dose - few can cause illness

62
Q

campylobacter treatment

A
  • not usually required
  • azithromycin (macrolide) is standard AB
  • resistance to fluoroquinolones is problematic
63
Q

campylobacter epidemiology

A

commonest cause of food poisoning in the UK

64
Q

features of e coli (gram -ve/+ve, how many pathotypes)

A
  • gram negative intestinal bacteria

- 6 pathotypes associated with diarrhoea

65
Q

enterotoxigenic e coli features and symptoms

A
  1. cholera-like toxin

2. watery diarrhoea

66
Q

enteroinvasive e coli features and symptoms

A

. shigella like illness

- bloody diarrhoea

67
Q

enterohaemorrhagic or shiga toxin producing E.coli e coli features and symptoms

A
  • ecoli O157 serogroup, shigatoxin/verotoxin

- 5-10% get haemolytic uraemic syndrome: loss of kidney function

68
Q

management of C diff in hosp

A
  • isolate patient
  • stop current ABs
  • metronidaloze, vancomycin
  • recurrence rate 15-35% aftr initial infection: increasingly hard to treat
  • faecal microbiota transplantation = 98% cure rate
  • remember metronidazole can cause c diff and gastroenteritis

BRS Year 2 (110 decks)

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