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LSS 2 - Abdomen, Alimentary and Urinary systems > AS Lecture 13 - Infection and Immunology of the Gut > Flashcards

AS Lecture 13 - Infection and Immunology of the Gut Flashcards

1
Q

What is the GIT immunology status?

A

Massive antigen load - resident microbiota, dietary antigens, exposure to pathogens State of restrained activation

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2
Q

What does immune homeostasis require?

A

Presence of bacterial microbiota

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3
Q

What are the 4 major phyla in the gut microbiota?

A

Bacteriodetes, Firmicutes, actinobacteria, proteobacteria

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4
Q

What are the abnormalities present in ‘germ-free’ animals - with no gut microbiota?

A

Immune function (oral tolerance) Metabolic function (altered enzymes) Physiological function (altered motility) Trophic function (altered cell turnover)

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5
Q

What are 4 infections of the GIT?

A

Oral candidiasis Helicobacter pylori Infective diarrhoea (bacterial, viral, amoebic) Clostridium difficile

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6
Q

What is oral canidiasis?

A

Yeast/fungal infection by Candida albicans Carried in 50% of individuals - asymptomatically usually

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7
Q

What patients are affected by oral candidiasis?

A

Immunocompromised patients

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8
Q

How is oral candidiasis treated?

A

With oral anti-fungals or IV antifungals is immunocompromised

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9
Q

What is helicobacter pylori?

A

GNB, microaerophilic rod

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10
Q

What are the symptoms of H. pylori?

A

Gastritis/ gastric or duodenal ulcers/ gastric carcinoma BUT 80% infected individuals are asymptomatic

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11
Q

How is H. pylori investigated and treated?

A

Investigated: Blood Ab, stool Ag, urea breath test, biopsy ureases test Treatment: 1 week eradication therapy with proton pump inhibitor and clarithromycin/amoxicillum

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12
Q

What are the main causes of traveller’s diarrhoea?

A

Escherichia coli (E coli) Shigella Salmonella Cholera Rotavirus Norovirus Giardia

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13
Q

What are the symptoms and transmission of Norovirus?

A

Acute gastroenteritis for less than 3 days with incubation of 24-48hrs Faeco-oral transmission Infectious for up to 2 weeks

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14
Q

What are the 4 strains of E. coli and what do they cause?

A

Enterotoxigenic - cholera-like toxin causing watery diarrhoea Enterhaemorrhagic - verotoxin/shigatoxin causing haemolytic uraemic syndrome Enteropathogenic - occurs in nurseries Enteroinvasive - shigella-like illness, bloody diarrhoea, megacolon

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15
Q

How does C. difficile colonise the colon?

A
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16
Q

What disease does C. difficile cause?

A

Pseudomembranous colitis (AB-associated colitis) A and B toxin

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17
Q

How is a C. difficile infection treated?

A

Isolate, stop current antibiotics and treat with metronidazole and vancomycin Then undergo faecal microbiota transplation

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18
Q

What is the success of faecal transplantation in C. difficile?

A

Cure rate of 98% - stool resembles donor stool in 2 weeks

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19
Q

How does the gut’s mucosal layer provide defense?

A

Physical barrier - epithelial and peristalsis, chemical (enzymes and pH) Commensal bacteria Immunological after invasion - MALT/GALT

20
Q

How does the epithelial layer act as a barrier?

A

Mucus layer (goblet cells) Epithelial monolayer (tight junctions, antimicrobial peptides and transports IgA) Paneth cells (bases of crypts and have defensins and lysozymes)

21
Q

Where are MALT most present?

A

In the oral cavity - the palatine tonsil, lingual tonsils and pharyngeal tonsil

22
Q

What is GALT and what are the 2 types?

A

Gut-associated lymphoid tissue - not organised OR organised

23
Q

What are some not organised GALT?

A

Intra-epithelial lymphocytes and lamina propria lymphocytes

24
Q

What are some organised GALT?

A

Cryptopatches, peyer’s patches, isolated lymphoid follicles, mesenteric lymph nodes

25
Q

What does GALT do?

A

Generates lymphoid cells and antibodies -> IgA (secretory and interstitial), IgG, IgM and cell mediated immunity

26
Q

What are peyer’s patches and where are they located?

A

Small intestine - mainly distal ileum (similar elsewhere in GIT) Covered by follicle associated epithelium (no goblet cells, secretory IgA, lack microvilli and infiltrated by T/B cells, macrophages and dendritic cells) Organised collection of naive T and B cells

27
Q

How do peyer’s patches develop?

A

Requires exposure to bacterial microbiota

28
Q

What is the structure of Peyer’s patches? FITB

A
29
Q

What is the function of peyer’s patches?

A

Antigen sampling by M cells Transport to APC in subepithelial dome, where DC’s take up Ag and process it They then present to naive B/T cells in Peyer’s patch or transport to lymph nodes - results in development on gut homing markers They then transfer to mesenteric lymph node to proliferate

30
Q

What is the B-cell adaptive response?

A

Naive B cells expressing IgM in peyer’s patches, which upon presentation switch to IgA, under influence from T cells and epithelium Then further maturation to become IgA secreting plasma cells, populating lamina propria

31
Q

What are intraepithelial lymphocytes?

A

Make up 1/5th of intestinal epithelium Made from: conventional T cells (lamina propria) - migrated from other tissue; unconventional T cells (innate) - resident, express unusual combinations of CD4/8 gamma/delta TCR Other innate immune cells - resident NK cells

32
Q

How is the T cell adaptive response activated and what does it lead to?

A

3 signals: presentation of Ag within MHC, co-stimulatory signals on DC and secretion of cytokines by DC Leads to: cell mediated immunity, normal gut response, inflammatory disease, tolerance

33
Q

What are the different types of T cells that can be formed from different IL stimulations?

A
34
Q

What is gut homing?

A

Lymphocytes proliferate in MLN and enter lymphatics to thoracic duct where they enter circulation, selectively home to sites similar to initial priming - Ag presentation in GALT favours gut homing characteristics (intergrins/chemokine receptors) Integrins act as a postcode marker so that the lymphocytes know to return to that site

35
Q

Why does the gut have a dual immunological role?

A

Immunoreactivity to pathogens BUT tolerance to food Ag and commensal bacteria

36
Q

What is immune tolerance?

A

Suppression of immune responses towards Ag via deletion of responding lymphocyte, anergy or TReg cells

37
Q

What may loss of tolerance underlie?

A

Inflammatory bowel disease Coeliac disease Food allergy

38
Q

What are some common food allegies?

A

Nuts Hen egg white Cows milk Wheat Sesame seeds Soya Shell fish

39
Q

What causes inflammatory bowel disease?

A

Genetic background, immune system and/or environmental factor With some factors like: smoking (sometimes the removal can cause bloody diarrhoea), stress, diet and vitamin D affecting

40
Q

What alleviates or worsens Crohn’s disease?

A

Faecal stream diversion alleviates but reanastomosis triggers recurrence Infusion of luminal contents into excluded normal bowel reduces inflammation

41
Q

Which gut flora are associated with certain symptoms of crohn’s disease?

A

Fusobacteriaceae - biomarker, progression of colorectal cancer Pastueurellacaea, Veillonellaceae, pathogenic E coli - linked with ulcer formation

42
Q

What does microaerophilic mean?

A

Needs a little bit of oxygen to survive

43
Q

How do dendritic cells sample the gut bacteria?

A

They stick their dendrites into epithelial barrier, so they can sample the lumen on the other side. It then takes the antigens to the MNL

44
Q

What is coeliac disease?

A

40-50% and most patients can be asymptomatic and others have bloating/abdominal pain, dermatitis

45
Q

How does coeliac disease present histologically?

A

Villus atrophy and many infiltration of intraepithelial lymphocytes

LSS 2 - Abdomen, Alimentary and Urinary systems (29 decks)

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