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BRS YR2 > Immunology of the Gut > Flashcards

Immunology of the Gut Flashcards

1
Q

What are the implications of the large surface area of the GI tract?

A

exposure to a massive antigen load

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2
Q

What does the massive antigen load consist of?

A
  • resident microbiota
  • dietary antigens
  • pathogen exposure
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3
Q

What is the impact of this large antigen load?

A

GI tract is in a state of ‘restrained activation’

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4
Q

What is a state of ‘restrained activation’

A
  • tolerance (food and commensal bacteria) vs active immune response
  • dual immunolgoical role
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5
Q

What does immune homeostasis and development of a healthy immune system require?

A

the presence of bacterial microbiota

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6
Q

What are the 4 major phyla of bacteria?

A
  • Bacteroidetes
  • Firmicutes
  • Actinobacteria
  • Proteobacteria
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7
Q

What is the benefits of the gut microbiota?

A
  • provides traits that we do not have in our genome
  • essential nutrients
  • metabolism of ingestible compounds
  • defence against colonisation of pathogens
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8
Q

What is dysbiosis?

A

altered microbiota composition

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9
Q

What is the impact of symbionts on the host?

A
  • no effect, truly neutral
  • for regulation
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10
Q

What is the impact of commensals on the host?

A

no effect, but benefit from being part of the host

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11
Q

What is the impact of pathobionts on the host?

A
  • no effect normally
  • can cause dysregulated inflammation and disease
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12
Q

What are the important factors of immunological equilibrium in the gut?

A
  • symbionts
  • commensals
  • pathobionts
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13
Q

What can cause dysbiosis?

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

What happens during dysbiosis?

A

production of bacterial metabolites and toxins

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15
Q

What are the 2 primary physical types of barriers?

A
  • Anatomical
  • Chemical
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16
Q

What are the different types of anatomical barriers?

A
  • epithelial barriers
  • peristalsis
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17
Q

What are the different types of chemical barriers?

A
  • enzymes
  • acidic pH
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18
Q

What is involved in the epithelial barrier?

A
  • mucus layer (goblet cells)
  • epithelial monolayer, tight junctions
  • paneth cells (in small intestines)
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19
Q

What is the role of Paneth Cells?

A
  • bases of crypts of Lieberkuhn
  • secrete antimicrobial peptides (defensins) and lysozyme
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20
Q

How do commensal bacteria act as barrier?

A

occupy an ecological niche

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21
Q

What is involved in the immunological barriers?

A
  • MALT (Mucosa Associated Lymphoid Tissue)
  • GALT (Gut Associated Lymphoid Tissue)
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22
Q

Where is MALT located?

A
  • in submucosa below the epithelium
  • as lymphoid mass containing lymphoid follicles
  • follicles are surrounded by HEV postcapillary venules (easy passage of lymphocytes for a response)
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23
Q

What area is rich in immunological tissue?

A

oral cavity

  • palatine tonsil
  • lingual tonsils
  • pharyngeal tonsils (adenoids)
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24
Q

What is the role of GALT?

A

adaptive and innate immune response through generations of lymphoid cells and Abs

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25
Q

What are the non-organised forms of GALT?

A
  • intra-epithelial lymphocytes (eg: T cells and NK cells)
  • Lamina propria lymphocytes
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26
Q

What are the organised forms of GALT?

A
  • Peyer’s patches
  • Caecal patches
  • Isolated lymphoid follicles
  • Mesenteric lymph nodes (encapsulated)
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27
Q

Where are Peyer’s patches found?

A

small intestine

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28
Q

Where are Caecal patches found?

A

large intestine

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29
Q

How are non-organised GALT released?

A

migrate to the tip of the microvilli prior to that as well as absorptive epithelial cells

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30
Q

What produces mucus secreting goblet cells?

A
  • stem cells
  • crypts
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31
Q

Where do Paneth cells migrate to?

A

the bottom of the crypt of Lieberkuhn

32
Q

Where are intraepithelial lymphocytes?

A

between entry sites

33
Q

What is found in the mucosa of the microvilli?

A
  • macrophages
  • IgA B cells
  • dendritic cells
  • T cells
34
Q

Where are Peyer’s patches?

A
  • submucosa small intestine
  • mainly in the distal ileum
35
Q

What are Peyer’s patches?

A

aggregated lymphoid follicles covered with follicle associated epithelium (FAE)

36
Q

What are characteristics of Peyer’s patches?

A
  • no goblet cells
  • no secretory IgA
  • lack microvilli
37
Q

What do Peyer’s patches contain?

A

Organised collection of naïve T cells and B-cells

38
Q

What is required for the development of Peyer’s patches?

A

exposure to bacterial microbiota

39
Q

How are antigens taken up by Peyer’s patches?

A
  • via M cells within FAE
  • expressIgA receptors, facilitating transfer of IgA-bacteria complexinto the Peyer’s patches
40
Q

What can trans-epithelial dendritic cells do?

A
  • open up tight junction proteins and send the dendrites outside into the lumen of the intestinal tract to directly sample bacteria
  • cells then go to mesenteric lymph nodes
41
Q

What happens in the B cell adaptive response in Peyer’s patches?

A
  • mature-naive B cells express IgM in Peyer’s patches
  • switch to IgA on antigen presentation
  • T cells and epithelial cells influence B cell maturation via cytokine production
  • B cells mature to become IgA secreting plasma cells
  • populate lamina propria
42
Q

How is secretory IgA produced?

A
  • plasma cell produces IgA
  • taken from submucosa into enterocyte vesicle
  • enzymatic cleavage
  • leading to secretory IgA in the lumen
43
Q

What does secretory IgA do?

A
  • bind to antigens in lumen
  • prevents adhesion and invasion
    (secreted by 90% of gut B cells)
44
Q

What happens in lymphocyte homing and circulation?

A
  • lymphocytes from Peyer’s patch move into the mesenteric lymphnode
  • proliferate in the lymphnode
  • return to circulation via the thoracic duct into the systemic venous system
  • can either enter the peripheral immune system or return to the intestinal mucosa via vessels in the lamine propria
45
Q

What is part of the peripheral immune system?

A
  • skin
  • tonsils
  • BALT (Bronchus Associated Lymphoid Tissue)
46
Q

How does the homing cascade direct circulating naive T cells to Peyer’s patches?

A
  • rolling adhesion of T cells to HEV
  • activation of T cells via binding of a4b7 integrin on T cell membrane and MAdCAM-1 on HEV walls
  • T cell secreted into the lamina propria
47
Q

Why do enterocytes and goblet cells have a rapid turnover?

A
  • first line of defense and may be directly affected by toxicity
  • may have impacts on function, metabolic rate
  • shorten the effect of lesions
48
Q

What happens if enterocyte and goblet cell turnover is interrupted?

A

severe intestinal dysfunction

49
Q

What is the mechanism behind cholera infections?

A
  • Vibrio cholerae serogroups O1 and O139
  • bacteria reaches small intestine, contact with epithelium triggers the release of cholera enterotoxin
  • cholera toxin enters cell via retrograde endocytosis
  • increased adenylate cyclase acitvity
  • increased cAMP
  • cAMP activates ion channels which secrete Na+, K+, Cl- and HCO3- into the intestinal lumen
  • water follows ions leading to osmotic diarrhoea
50
Q

How is cholera transmitted?

A
  • faecal-oral route (contaminated water and food)
51
Q

What are the main symptoms of cholera?

A
  • severe dehydration
  • watery diarrhoea
  • vomiting
  • nausea
  • abdominal pain
52
Q

How do you diagnose cholera?

A
  • bacterial culture from stool sample on selective agar (gold standard)
  • rapid dipstick tests
53
Q

How do you treat cholera?

A

oral rehydration

54
Q

How do you vaccinate against cholera?

A
  • Dukoral vaccine
  • oral and inactivated
55
Q

What are the possible viral causes of infectious diarrhoea/gastroenteritis?

A
  • Rotavirus (children)
  • Norovirus
56
Q

What are the possible bacterial causes of infectious diarrhoea/gastroenteritis?

A
  • Campylobacter jejuni
  • E. coli
  • Salmonella
  • Shigella
  • C. difficile
57
Q

What are the possible protozoal parasitic causes of infectious diarrhoea/gastroenteritis?

A
  • Giardia lamblia
  • Entamoeba histolytica
58
Q

What are rotaviruses?

A
  • RNA virus
  • replicates in enterocytes
  • 5 types (A-E)
  • A most common in human infection
59
Q

How common are rotaviruses?

A

most common cause of diarrhoea in children and infants

60
Q

How do you treat rotaviruses?

A
  • oral rehydration therapy
  • Rotarix vaccination (live, attenuated against type A)
61
Q

What is Norovirus?

A
  • RNA virus
  • incubation: 24-48hours
62
Q

How are Noroviruses transmitted?

A
  • faecal-oral transmission
  • may shed virus for up to 2 weeks
  • outbreaks in closed communities common
63
Q

What are the symptoms of Norovirus?

A
  • acute gastroenteritis
  • recovery in 1-3 days
64
Q

How do you diagnose Norovirus?

A

Sample PCR

65
Q

What are the causes of food poisoning?

A
  • Campylobacter jejuni
  • Campylobacter coli
66
Q

How is Campylobacter transmitted?

A
  • undercooked meat
  • untreated water
  • un-pasturised milk
  • low infective dose
67
Q

How do you treat for Campylobacter?

A
  • not usually required
  • Azithromycin is standard ABx
  • Resistance to fluoroquinolones is problematic
68
Q

What are the pathotypes of E. coli?

A

gram negative bacteria

  • Enterotoxic E. coli
  • Enterohaemorrhagic/Shiga toxin-producing E. coli
  • Enteroinvasive E. coli
  • Enteropathogenic E. coli
  • Enteroaggregative E. coli
  • Diffusely adherent E. coli
69
Q

What symptoms is Enterotoxic E. coli associated with?

A
  • cholera like toxin
  • water diarrhoea
70
Q

What symptoms is Enterohaemorrhagic/Shiga toxin-producing E. coli associated with?

A
  • 5-10% haemolytic uraemic syndrome
  • loss of kidney function
71
Q

What symptoms is Enteroinvasive E. coli associated with?

A
  • shigella like illness
  • bloody diarrhoea
72
Q

How does Clostridium difficile infect the body?

A
  • always present in the gut
  • exogenous disturbance e.g. antibiotics leads to dysbiosis
  • intermediate dysbiotic state
  • pathogen induced disturbance and toxin induction leads to diseased state
73
Q

How do you manage Clostridium difficile?

A
  • isolation
  • stop current ABx
  • Metronidazole (can also trigger infection)
  • Vancomycin
  • reccurence rate 15-35%, increasingly more difficult to treat
  • faecal microbiota transplant
74
Q

What symptoms would indicate a C. difficile infection?

A
  • raised WCC and CRP
  • new onset diarrhoea
  • generalised tenderness
  • signs of dehydration (AKI and dry mucous membranes)
75
Q

How do you diagnose a C. difficile infection?

A
  • stool sample for C. difficile toxin
  • stool cultures
  • Imaging (AXR)

BRS YR2 (67 decks)

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