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Z YEAR 2 BRS GASTRO > Gut Immunology > Flashcards

Gut Immunology Flashcards

1
Q

What is the surface area of the GI tract?

A

200m^2

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2
Q

What is the state of the GI tract?

A

State of “restrained activation”

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3
Q

Why is bacterial microbiota important?

A

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

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4
Q

What is tolerance?

A
  • food antigens

- commensal bacteria

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5
Q

What is the massive antigen load that the GI tract needs to deal with?

A
  • Resident microbiota 1014 bacteria
  • Dietary antigens
  • Exposure to pathogens
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6
Q

What is immunoreactivity?

A

pathogens

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7
Q

What is involved in GI tract immunology?

A

– Tolerance vs active immune response

– Dual immunological role

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8
Q

How many gut bacteria and cells are there?

A

10^14 gut bacteria and 10^13 cells in the body

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9
Q

What are the 4 major phyla of bacteria?

A
  1. Bacteriodetes
  2. Firmicutes
  3. Actinobacteria
  4. Proteobacteria
    - also viruses and fungi
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10
Q

Why do we need the gut microbiota?

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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11
Q

What is dysbiosis?

A

altered microbiota composition

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12
Q

What is all balanced in immunological equilibrium?

A
  1. Symbionts (regulation): live with host no benefits/harm
  2. Commensals: benefits from host but no affect on host
  3. Pathobionts (inflammation): can cause inflammation and disease in certain circumstance but usually symbionts
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13
Q

Which bacterial metabolites and toxins can be produced by pathobiomes in dysbiosis?

A
  • TMAO
  • 4-EPS
  • SCFAs
  • bile acids
  • AHR ligand
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14
Q

What are the brain diseases that can develop from dysbiosis?

A
  1. Stress
  2. Autism
  3. Multiple sclerosis
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15
Q

What are the lung diseases that can develop from dysbiosis?

A

asthma

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16
Q

What are the liver diseases that can develop from dysbiosis?

A
  1. NAFLD

2. NASH

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17
Q

What are the adipose tissue diseases that can develop from dysbiosis?

A
  1. Obesity

2. Metabolic disease

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18
Q

What are the intestine diseases that can develop from dysbiosis?

A
  1. IBD

2. Coeliac disease

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19
Q

What are the systemic diseases that can develop from dysbiosis?

A
  1. T1 diabetes
  2. Atheroscelerosis
  3. Rhematoid arthritis
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20
Q

What aspects can contribute to both healthy microbiota and dysbiosis?

A
  1. Infection or inflammation
  2. Diet
  3. Xenobiotics
  4. Hygiene
  5. Genetics
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21
Q

What are the anatomical physcial barriers to muscosal defence?

A
  • Epithelial barrier

* Peristalsis

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22
Q

What are the chemical physcial barriers to muscosal defence?

A
  • Enzymes

* Acidic pH

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23
Q

What are commensal bacteria?

A

occupy “ecological niche”

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24
Q

What is an immunological response to invasion?

A

following invasion
•MALT (Mucosa Associated Lymphoid Tissue)
•GALT (Gut Associated Lymphoid Tissue)

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25
Q

What is the epithelial barrier made up of?

A
  1. Mucus layer - Goblet cells
  2. Epithelial monolayer - Tight junctions
  3. Paneth Cells (small intestine)
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26
Q

What are Paneth Cells? Where are they?

A

-small intestine
•Bases of crypts of Lieberkühn
•Secrete antimicrobial peptides (defensins) & lysozyme

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27
Q

Where is MALT found?

A

in the submucosa below the epithelium, as lymphoid mass containing lymphoid follicles

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28
Q

What are the follicles in MALT surrounded by?

A

surrounded by HEV postcapillary venules, allowing easy passage of lymphocytes

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29
Q

What is the oral cavity rich in?

A

immunological tissue

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30
Q

What is GALT responsible for?

A

adaptive and innate immune system

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31
Q

What does GALT consist of?

A
  1. B and T lymphocytes
  2. Macrophages
  3. APC (dendritic cells)
  4. Specific epithelial and intra epithelial lymphocytes
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32
Q

What is the non organised section of GALT?

A
  1. Intra-epithelial lymphocytes
    •Make up 1/5th of intestinal epithelium, e.g. T-cells, NK cells
  2. Lamina propria lymphocytes
33
Q

What is the organised section of GALT?

A
  1. Peyer’s patches (small intestine)
  2. Caecal patches (large intestine)
  3. Isolated lymphoid follicles
  4. Mesenteric lymph nodes (encapsulated)
34
Q

Where are peyer’s patches found?

A

in submucosa small intestine – mainly distal ileum

35
Q

What are stimulatory factors for microbiota?

A
  1. Ingested nutrients
  2. Secreted nutrients
    - lead to bacterial growth
36
Q

What are inhibitory factors for microbiota?

A
  1. Chemical digestive factors (bacterial lysis)

2. Peristalsis, contractions and defecation (bacterial elimination)

37
Q

What is dysbiosis?

A
  • immunological dysequilbrium

- Altered microbiota composition

38
Q

What are the aggregated lymphoid follicles covered with in peyers patches?

A

with follicle associated epithelium (FAE)

39
Q

What is FAE?

A

no goblet cells, no secretory IgA, no microvilli

40
Q

What is Peyer’s Patches?

A

Organised collection of naïve T cells & B-cells

41
Q

What is needed for the development of Peyer’s Patches?

A

-requires exposure to bacterial microbiota

•50 in last trimester foetus, 250 by teens

42
Q

What are M cells in Peyer’s patches?

A
  • Antigen uptake via M (microfold) cells within FAE

* M cells expressIgA receptors, facilitating transfer of IgA-bacteria complexinto the Peyer’s patches.

43
Q

What do mature naive B cells express in Peyer’s patches?

A

IgM

44
Q

What happens to the IgM on antigen presentation?

A

class switches to IgA

45
Q

What influences B cell maturation? What do they populate?

A
  1. T-cells & epithelial cells influence B cell maturation via cytokine production
  2. B cells further mature to become IgA secreting plasma cells.
  3. Populate lamina propria
46
Q

What is the formation of IgA?

A

Up to 90% of gut B-cells secrete IgA

47
Q

Where does sIgA bind (secretory IgA)?

A
  • sIgA binds luminal antigen

* → preventing its adhesion and consequent invasion.

48
Q

Why if enterocytes & goblet cells of small bowel have a short life span (about 36 hrs)
and rapid turnover contrasts with lifespan of weeks/months for other epithelial cell types (e.g. lung, blood vessels)?

A
  1. Enterocytes are first line of defense against GI pathogens & may be directly affected by toxic substances in diet
  2. Effects of agents which interfere with cell function, metabolic rate etc will be diminished.
  3. Any lesions will be short-lived.
49
Q

What is the mechanism of cholera infection?

A
  1. Cholera -acute bacterial disease caused by Vibrio cholerae serogroups O1 & O139
  2. Bacteria reaches small intestine → contactwith epithelium & releasescholera enterotoxin
50
Q

How is cholera transmitted?

A
  • Transmitted through faecal-oral route

* Spreads via contaminated water & food

51
Q

What are the symptoms of cholera?

A
  1. Main symptoms
    •Severe dehydration & watery diarrhoea
  2. Other symptoms
    Vomiting, nausea & abdominal pain
52
Q

What does the diagnosis of cholera involve?

A

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

53
Q

What does the treatment of cholera involve?

A

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

54
Q

Is there a vaccine for cholera?

A

Dukoral, oral, inactivated

55
Q

What is the epidemiology of cholera?

A

Globally 1.3 - 4 million cases, avg. 95,000 deaths/year (last indigenous UK case 1893: 2017 - 13 cases)

56
Q

What are the viral causes of infectious diarrhoea?

A
  • Rotavirus (children)

* Norovirus “winter vomiting bug”

57
Q

What are the protozoal parasitic causes of infectious diarrhoea?

A
  • Giardia lamblia

- Entamoeba histolytica

58
Q

What are the bacterial causes of infectious diarrhoea?

A
  1. Campylobacter jejuni
  2. Escherichia coli
  3. Salmonella
  4. Shigella
  5. Clostridium difficile
59
Q

What is rotavirus?

A
  • RNA virus, replicates in enterocytes.

* 5 types A – E, type A most common in human infections.

60
Q

What is the epidemiology of rotaviruses?

A

Most common cause of diarrhoea in infants & young children worldwide

61
Q

What is the treatment of rotaviruses?

A
  1. Oral rehydration therapy
  2. Still causes ~ 200,000 deaths/year.
  3. Before vaccine, most individuals had an infection by age 5, repeated infections develop immunity.
62
Q

Is there a vaccination for rotaviruses?

A

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

63
Q

What is norovirus?

A
  • RNA virus

* Incubation period 24-48 hours

64
Q

What is the transmisstion of norovirus?

A
  1. Faecal-oral transmission.
  2. Individuals may shed infectious virus for up to 2 weeks
  3. Outbreaks often occur in closed communities
65
Q

What are the symptoms of norovirus?

A

•Acute gastroenteritis, recovery 1 – 3 days

66
Q

What is the treatment of norovirus?

A

•Not usually required

67
Q

What is the diagnosis of norovirus?

A

•Sample PCR.

68
Q

What is the epideimiology of norovirus?

A

•Estimated 685 million cases per year.

69
Q

What is the most common species of campylobacter?

A

•Campylobacter jejuni, Campylobacter coli

70
Q

What is the transmission of campylobacter?

A
  • Undercooked meat (especially poultry), untreated water & unpasteurised milk
  • Low infective dose, a few bacteria (<500) can cause illness
71
Q

What is the treatment of campylobacter?

A
  1. Not usually required
  2. Azithromycin (macrolide) is standard antibiotic
  3. Resistance to fluoroquinolones is problematic
72
Q

What is the epidemiology of campylobacter?

A
  • Estimated 280,000 cases per year in UK, 65,000 confirmed

* Commonest cause of food poisoning in the UK

73
Q

What is E.Coli?

A

•Diverse group of Gram-negative intestinal bacteria
•Most harmless
6 ”pathotypes” associated with diarrhoea (diarrhoeagenic)

74
Q

What is Enterotoxigenic E. coli (ETEC)?

A
  • Cholera like toxin

* Watery diarrhoea

75
Q

What is Enterohaemorrhagic or Shiga toxin-producing E. coli (EHEC/STEC)?

A
  • E. coli O157 serogroup, Shigatoxin/verotoxin

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

76
Q

What is Enteroinvasive E. coli (EIEC)?

A
  • Shigella like illness

* Bloody diarrhea

77
Q

What are other pathotypes of E coli?

A

•Enteropathogenic E. coli (EPEC)
•Enteroaggregative E. coli (EAEC)
-Diffusely adherent E. coli (DAEC

78
Q

What is the management of Clostridium Difficile?

A
  1. Isolate patient (very contagious)
  2. Stop current antibiotics
  3. Metronidazole, Vancomycin
  4. Recurrence rate 15-35% after initial infection, increasingly difficult to treat.
  5. Faecal Microbiota Transplantation (FMT) – 98% cure rate

Z YEAR 2 BRS GASTRO (15 decks)

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