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Gastroenterology > Gut Immunology > Flashcards

Gut Immunology Flashcards

1
Q

GI tract balance

A

State of ‘restrained activation’

  • tolerance vs active immune response
  • dual immunological role
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2
Q

‘Virtual’ organ

A

Microbiota

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3
Q

Factors that stimulate bacterial growth

A

Ingested nutrients

Secreted nutrients

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4
Q

Factors that stimulate bacterial lysis or elimination

A

Chemical digestive factors

Peristalsis, contractions, defecation

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5
Q

Chemical digestive factors in stomach

A

HCl
Pepsin
Gastric lipase

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6
Q

Chemical digestive factors in liver

A

Bile acid

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7
Q

Chemical digestive factors in pancreas

A

Trypsin
Amylase
Carboxypeptidase

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8
Q

Chemical digestive factors in small intestine

A

Brush border enzymes

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9
Q

Chemical digestive factors in colon

A

None

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10
Q

Bacterial content in stomach

A

10^1

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11
Q

Bacterial content in duodenum

A

10^3

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12
Q

Bacterial content in jejunum

A

10^4

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13
Q

Bacterial content in ileum

A

10^7

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14
Q

Bacterial content in colon

A

10^12

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15
Q

Immunological equilibrium

A

Symbionts, commensals, pathobionts

Balance tips to inflammation when pathogens are involved with pathobionts - dysbiosis

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16
Q

Factors that may cause dysbiosis

A 
Infection or inflammation
Diet
Xenobiotics 
Hygiene
Genetics
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17
Q

Mucosal defense - physical barrier

A

Anatomical - epithelial barrier and peristalsis

Chemical - enzymes and acidic pH

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18
Q

Epithelial barrier

A

Mucus layer made by goblet cells

Epithelial monolayer by tight junctions

Paneth cells

  • bases of crypts of Lieberkühn
  • secrete antimicrobial peptides (defensins) and lysozyme
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19
Q

Mucosal defense - other barrier

A

Commensal bacteria - occupy ‘ecological niche’

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20
Q

Mucosal defense - immunological

A

Following invasion

MALT - mucosa associated lymphoid tissue
GALT - gut associated lymphoid tissue

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21
Q

MALT

A

Found in submucosa below epithelium. Exist as lymphoid mass containing lymphoid follicles.
Follicles are surrounded by HEV postcapillary venules, allowing easy passage of lymphocytes

Oral cavity is rich in immunological tissue

  • palatine tonsil
  • lingual tonsil
  • pharyngeal tonsils (adenoids)
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22
Q

GALT

A

Responsible for both adaptive and innate immune responses
Consist of B and T lymphocytes, macrophages, APC (dendritic cells), and specific epithelial and intra-epithelial lymphocytes

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23
Q

Non organised GALT

A

Intra-epithelial lymphocytes
-make up 1/5 of intestinal epithelium - T-cells, NK cells etc.
Lamina propria lymphocytes

24
Q

Organised GALT

A

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

25
Q

Stem cell of intestine location

A

In crypts

26
Q

Commonest cells of intestine

A

Enterocytes (intestinal epithelial cells)

Migrate towards tip of villi

27
Q

Goblet cells

A

Mucus secreting

Cell of intestine

28
Q

Paneth cells

A

Migrate to bottom of crypt

Characterised by presence of dense granules and antimicrobial peptides

29
Q

Lamina propria lymphocytes

A

Central part of villus

T cell, macrophages, dendritic cells, IgA B cells

30
Q

Intraepithelial lymphocytes

A

Dotted between enterocytes

31
Q

Peyer’s patches

A

Found in submucosa small intestine - mainly distal ileum
Aggregated lymph’s follicles covered with follicle associated epithelium (FAE - no goblet cells, no secretory IgA, lack microvilli)
Organised collection of naive T cells and B cells, and subepithelial dome of dendritic cells
Development requires exposure to bacterial microbiota - 50 in last trimester fetus, 250 by teens
Antigen uptake via M (microfold) cells within FAE
M cells express IgA receptors, facilitating transfer of IgA bacteria complex into Peyer’s patches

32
Q

Antigen sampling

A

M cells
Dendritic cells - open up tight junctions to send dendrites into lumen to sample bacteria and bring back to transport to mesenteric lymph nodes

33
Q

B cell adaptive response

A

Pathogen taken up by M cells
Excreted into pocket formed in inner surface of enterocytes which contains antigen presenting cells such as dendritic cells
Antigen engulfed and presented to MHC II molecules on surface
Dendritic cells then migrate to Peyer’s patch
DC, T and B cells all aggregate in patch and form an organised lymphoid follicle
Other antigen loaded dendritic cells escape and migrate through lymphatic system where they activate B cells, T cells, other plasma cells in mesenteric lymph nodes
Some activated cells then return to GALT tissue effector sites and produce antibodies secreted from intestinal lumen

34
Q

B cell maturation

A 
Mature naive B cells express IgM in Peyer’s patches 
On antigen presentation class switched to IgA

T cells and epithelial cells influence B cell maturation via cytokine production
B cells further mature to become IgA secreting plasma cells
Populate lamina propria

35
Q

Secretory IgA

A

Up to 90% of gut B cells secrete IgA

sIgA binds luminal antigen - preventing adhesion and consequent invasion

36
Q

Lymphocyte homing and circulation

A

Lymphocytes travel to mesenteric lymph nodes - lymphocyte proliferation - return to circulation via thoracic duct
Either enter peripheral immune system (skin, tonsils, bronchus associated lymphoid tissue) or exit peripheral immune system and return to intestinal mucosa via vessels in lamina propria

37
Q

Cholera mechanism

A

Acute bacterial disease caused by vibrio cholerae serogroupd O1 and O139
Bacteria reaches small intestine - contact with epithelium and releases cholera enterotoxin via retrograde endocytosis
Once inside it increases adenylate cyclase activity - increased cAMP - active secretion of salt, potassium, chloride, bicarbonate - water follows

38
Q

Cholera transmission

A

Faecal oral - spreads via contaminated water and food

39
Q

Cholera symptoms

A

Severe dehydration and watery diarrhoea

Vomiting, nausea, and abdominal pain

40
Q

Cholera diagnosis

A

Bacterial culture from stool sample, selective agar is standard, rapid dipstick also available

41
Q

Cholera treatment

A

Oral rehydration is main management
Up to 80% get better by itself
Vaccine

42
Q

Other causes of infectious diarrhoea (gastroenteritis)

A

Viral

  • Rotavirus (children)
  • norovirus

Bacterial

  • salmonella
  • shigella
  • c.diff
43
Q

Rotavirus

A

RNA virus, replicates in enterocytes

Five types A-E, A most common in Human infections

44
Q

Rotavirus treatment

A

Oral rehydration therapy

Vaccine - live attenuated oral vaccine (Rotarix) against type A

45
Q

Norovirus Norwalk virus

A

RNA virus

Incubation 24-48 hours

46
Q

Norovirus Norwalk transmission

A

Faecal oral
May shed infectious virus for up to 2 weeks
Outbreaks often in closed communities

47
Q

Norovirus Norwalk symptoms

A

Acute gastroenteritis, recovery 1-3 dats

48
Q

Norovirus Norwalk treatment

A

Not required

49
Q

Norovirus Norwalk diagnosis

A

Sample PCR

50
Q

Campylobacter

A

Curved bacteria

Jejuni or coli

51
Q

Campylobacter transmission

A

Undercooked meat, untreated water and unpasteurised milk

Low ineffective dose, a few bacteria can cause illness

52
Q

Campylobacter treatment

A

Not required

Azithromycin standard antibiotic

53
Q

E. Coli

A 
Diverse group of gram negative intestinal bacteria 
Most harmless 
6 pathotypes associated with diarrhoea 
EHEC/STEC most problematic 
ETEC
EIEC
EPEC
EAEC
DAEC
54
Q

C. Diff

A

More C. Diff than normal leads gut from health stable state to intermediate dysbiotic state
Could either go back to recovery or diseased state where pathogen induced disturbance (toxin production) create supportive environment

55
Q

C. Diff management

A

Isolate patient - very contagious
Stop current antibiotic - caused by antibiotics
Metronidazole or vancomycin
Recurrence rate 15-35% after initial infection, increasingly difficult to treat
Faecal microbiota transplantation (FMT) 98% cure rate

Gastroenterology (11 decks)

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