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Alimentary system > Infection and immunology of the gut > Flashcards

Infection and immunology of the gut Flashcards

1
Q

Why are there so many bacteria in the gut?

A

Massive antigen load:

  • external pathogens
  • dietary antigens
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2
Q

What state is the gut immune system in?

A

The gut immune system is in a restrained state - tolerance vs active immunity

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3
Q

What are the most prevalent bacteria in the gut, especially the colon?

A

bacteroidetes

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4
Q

What are the functions of the microbiota?

A
  • oral tolerance
  • enzyme alteration
  • motility alteration
  • alteration of cell turnover
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5
Q

What are some features of the microbiome?

A
  • 10,000 different types of organisms
  • diverse types between humans
  • diet, host genetics and early microbial exposure affect repertoire
  • different body site have unique communities
  • at particular sites microbe have similar genes/functions
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6
Q

Describe the distribution of microbiota in GI tract

A
  • Loads in the mouth is because we put lots of dirty things into it, including food, fluid, cutlery, air etc.
  • Into the stomach, the low pH kills lots of bacterial populations so near 0 (except H. pylori)
  • The number is kept low in the duodenum, jejunum and proximal ileum because of paneth cells and Peyer’s patches
  • Beyond the ileocaecal valve the number of microorganisms increases markedly
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7
Q

Helicobacter pylori: what is it , what does it cause and treatment?

A
  • gram negative, rod
  • in response to H.Pylori excess acid production which causes the damage
  • in chronic cases, atrophy of stomach wall and malignant growths
  • causes: gastritis, gastric or duodenal ulcers, gastric carcinoma
  • investigations include blood antibodies, stool antigen, urea test, breath test
  • treatment is 1 week with proton pump inhibitor and amoxicillin
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8
Q

Traveller’s diarrhoea

A

Bacterial, viral and ameobic

  • bacteria: E.coli, shigella, salmonella and cholera
  • viral: rotavirus, norovirus (most common are viruses)
  • ameobic: giardia
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9
Q

Norovirus, incubation period and length of infectiousness

A

causes acute gastroenteritis in less than 3 days, in 24-48 hrs incubation and infectious for up to 2 weeks

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10
Q

What are the types of diarrhoea caused by different E.coli types?

A

enterotoxigenic E. coli (watery)
enterohaemorrhagic
enteropathogenic
enteroevasive (bloody)e

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11
Q

Clostridium difficile

A
  • antibiotics kill commensals and this is able to produce toxins causing mucosal injury
  • then neutrophils and RBC leak into the gut
  • Produces toxins A and B
  • results in pseudomembranous colitis
  • treatment include isolating, stopping AB, vanocmycin, faecomicrobiota transplantation
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12
Q

Mucosal defence - 3 types?

A
  • physical (anatomical: epithelial layer, peristalsis and chemical: pH, enzymes)
  • commensal bacteria
  • immunological (MALT, GALT)
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13
Q

The structure and function of the epithelial barrier

A
  • mucus secreted by goblet cells, maintained by glycocalyx
  • monolayer has tight junctions, antimicrobial peptides and IgA
  • paneth cells in crypts secrete lysozymes and defensins
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14
Q

Organisation of GALT

A

seperated into organised and non organised:

Organised: cryptopatches, peyer’s patches (SI), isolated lymphoid follicles (colon), mesenteric lymph nodes

Non organised: floats randomly in sub epithelial e.g. intra epithelial lymphocytes and lamina propria lymphocytes

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15
Q

What is the function of GALT?

A

generate lymphoid cells and antibodies and cell mediated immunity

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16
Q 
GALT - Peyer's patch
where is it
when does it develop
what does it consist of
what is present and not
A
  • found in distal ileum
  • develops throughout life into teens
  • has B cell and T cells areas
  • covered by follicle associated epithelium
  • has no goblet cells, IgA, microvilli
  • infiltrated by T/B cells, macrophages and dendritic cells
  • antigen taken up by M cell on epithelium
  • similar found in colon
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17
Q

What do mature naive B cells express in PP?

A 
IgM and class switch to IgA
They populate lamina propria
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18
Q

IgA antibody

A
  • upto 90% of gut B cells make this
  • dimeric at mucosa
  • prevents invasion, adherence and does not activate complement or Tc cells
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19
Q

T cells adaptive response - 3 signals

A

Determined by 3 signals:

  • presentation of antigen MHC by DC
  • costimulatory signal from DC
  • secretion of cytokines by DC
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20
Q

Give examples of some types of T cells

A

th1 - cellular, automimmunity
th2 - humoural e.g asthma
th17 - inflammation, autoimmunity
iTreg

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21
Q

Pathway of lymphocytes after activation

A

proliferate in mesenteric lymph node -> thoracic duct -> circulation -> go to sites similar to where they were activated

22
Q

What regulates T cell homing (know where they are from and can return)

A
  • T cells exhibits alpha4beta7 intergin
  • gut epithelium exhibits MAdCAM -1
  • Interaction between the two means t cells specific to gut
23
Q

What may loss of tolerance cause?

A
  • inflammatory bowel disease
  • coeliac disease
  • food allergies
24
Q

Coeliac disease histology

A
  • villus atrophy so less absorption

- large infiltrate of intra epithelial lymphocytes

25
Q

Pathogenesis of coeliac disease

A
  • MHC has two hit model of mutation in DQ2 or DQ8
  • grains like gluten stimulate AP cells to activate CD4 t cells and macrophages with IL-15 which causes epithelial remodelling and atrophy
26
Q

Presentation of coeliac disease and treatment

A
  • anaemia
  • malnourished
  • diarrhoea
  • bloating
  • scurvy/osteoporosis
  • steatorrhoea
treatment:
diet restriction (gluten free)
27
Q

Inflammatory bowel disease- Chron’s and ulcerative colitis, what is it?

A
  • inappropriate chronic immune response against gut microbes
28
Q

Incidence and trends in ulcerative colitis and Chron’s

A
  • UC has higher incidence but Chron’s incidence is increasing more
  • Incidence increasing in young and non western countries
29
Q

Which 4 factors contribute to the effects of IBD?

A
  • smoking (smoking cessation worsens UC and smoking worsens Chron’s)
  • stress
  • diet
  • vitamin D
30
Q

What are some changes occurring in Chron’s disease?

A
  • dysbiosis - reduction in diversity, anterobacteriacea and reminococcus gnavus rise and drop in clostridium types
  • rise in fusobacteriacea which can progress to colorectal cancer
  • rise in pastuerellacaea, veillonellaceae and pathogenic E coli
31
Q

What are some changes occurring in UC?

A

decreases in faecalibacacterium praunsnitzii and reseburai hominus

32
Q

What are the overall changes in the microbiome in IBD (not organisms)?

A
  • change in oxidative stress pathways
  • decreased carbohydrate metabolism
  • decreased amino acid synthesis
  • in ilieal Chron’s increase in virulence and secretion pathways
33
Q

Virome in IBD?

A

Expansion of caudovirales and bacteriophages

34
Q

Fungal microbiota in IBD?

A

there is some

35
Q

Treatment for IBD

A

immune targets

  • CAM inhibitors
  • TNF alpha inhibitos
  • JaK3 inhibitors
36
Q

What is the function and importance of M cells?

A
  • FAE contains specialized enterocytes or M cells
  • The main function of M cells is to perform transcytosis of luminal bacteria, antigens and proteins
  • M cells express IgA receptors, facilitating transfer of IgA-bacteria compex into the peyer’s patches
  • Antigen uptake is a combined effort by specialised M-cells and dendritic cells
37
Q

IgA dimer secretion

A
  • SIgA is a dimeric form of IgA - In the plasma cell, two IgA molecules are bound together by a J-chain, and secreted into the interstitial space.
  • The dimer binds to a special receptor on the external basolateral surface of enterocytes
  • This receptor becomes the secretory component and binds to the length of the IgA dimer, becoming SIgA
  • SIgA is then endocytosed into the epithelial cell and actively transported within a vesicle to the apical membrane, where it is exocytosed into the gut lumen.
  • The secretory component protects the antibody dimer from enzymatic and acidic degradation
38
Q

How do lymphocytes exit circulation?

A
  • L-selectin is expressed on the surface of lymphocytes and mediates the low adhesive interactions that enable leukocytes to roll in postcapillary venules and HEVs
  • In HEVs, L-selectin binds to (MAdCAM-1)
  • In addition to the HEVs of Peyer’s patches and mesenteric lymph nodes, MAdCAM-1 is expressed on the endothelial cells localised in the lamina propria of the small and large intestine and enables lymphocyte recruitment
39
Q

Where can MAdCAM-1 be found?

A

HEVs of Peyer’s patches and mesenteric lymph nodes

On endothelial cells localised in the lamina propria of the small and large intestine

40
Q

What are some symptoms of irritable bowel syndrome?

A
  • Recurrent abdominal pain
  • Abnormal bowel motility
  • Constipation and/or diarrhea
41
Q

What are the treatments for IBS?

A

Diet modification - Avoiding certain foods such as apples, beans, cauliflowers

Treatment of constipation - soluble fiber, stool softeners and osmotic laxatives

Treatment of spasms and pain - anti-diarrheals, anti-muscarinic

Management of stress, anxiety, depression

42
Q

What are some triggers for IBS?

A

Acute gastreoenteritis, stress

43
Q

What causes pain in IBS and diarrhoea?

A

Short chain carbohydrates trigger symptoms - maybe unabsorbed ones act as solutes leading to diarrhoea. They are metabolised by bacteria causing gas.

44
Q

Mechanism behind coeliac disease

A
  • Gliadin (component of gluten) is not broken down in the stomach, reaches the small intestine, and binds to the secretory IgA in the mucosal membrane.
  • Gliadin-secretory IgA complex binds to the Transferrin receptor (TFR) and are transferred to the lamina propria.
  • Enzyme tissue transglutaminase (tTG) cuts off amide group from the protein.
  • Deamidated gliadin is phagocytosed by the macrophages, and presented by MHC II molecules.
  • This leads to activation of immune system causing destruction of epithelial cells.
45
Q

How is coeliac disease diagnosed?

A
  • Antibody blood tests (anti-gliadin, anti-tTg, anti-endomysial)
  • Biopsy test of duodenum
46
Q

What is thought to be responsible for chron’s disease?

A

Frame-shift mutation in NOD2 gene

Immune-related disorder - triggered by pathogens such as mycobacterium paratuberculosis, pseudomonas, and listeria

Unregulated immune response causing the destruction of cells in the GI tract.

47
Q

Treatment for Chron’s

A
  • anti inflammatory drugs, antibiotics
  • immunosuppressants
  • remove tissue
  • liquid diet
  • food intolerance tests
48
Q

Mechanism of UC?

A

Autoimmune disorder - T cells destroy the cells lining the walls of large intestine
Secondary cause - Diet and stress

49
Q

Treatment for UC?

A
  • anti inflammatory drugs
  • immunosuppressant
  • colectomy
  • diet changes
  • pre/probiotcs
  • drink fluids and nutritional drinks for diarrhoea
50
Q

Cholera: symptoms, mechanism, diagnosis and treatment

A

symptoms:

  • vomiting
  • abdominal pain
  • diarrhoea

mechanism:

  • The bacteria reaches the small intestine from the stomach, where the flagellum propels it towards the epithelial cell.
  • On making close contact it releases cholera toxin.
  • Cholera toxin on entering the epithelial cell, starts a series of biochemical reactions resulting in exit of ions such as Na+, K+, Cl- and water from the epithelial cell.

diagnosis:
stool test

treatment:

  • Drink a lot of fluids.
  • Antibiotics?
  • Vaccination for cholera is also available.

Alimentary system (14 decks)

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