Immunology Of The GI Tract Flashcards

1
Q

MALT definition

A

Mucosal surfaces that are exposed to external infectious agents.
- therefore these areas need lymphoid tissues at these areas to combat immediately

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2
Q

GALT

A

Specialized epithelial cells and their products that are found in the GI tract.
- specifically in the Lamina propria layer for he GI tract

Possesses scattered IELs with intraepithelial lymphocytes. Specifically CD8+ T-cells

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3
Q

What are regional/sentinel lymph nodes for most GALT tissues?

A

Mesenteric lymph nodes

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4
Q

What areas of the gut tract possess highest thickness levels of mucus?

A

From highest to lowest

Colon

Ileum

Antrum of stomach

Duodenum and corpus of the stomach

Jejunum

corpus/antrum of stomach and the terminal colon are the only sites for firmly adherent mucus, the rest is loosely adherent

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5
Q

Goblet cells vs paneth cells

A

Both are found in the GALT tissues and throughout GI tract

Goblet:

  • produces mucus
  • inner layer of mucus = defenses and IgA are adhered
  • outer layer of mucus = comensal bacteria are adhered

Paneth cells
- produce defensins (usually into crypts for them to float around in the GU tract and adhere to mucus)

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6
Q

Crohn’s disease pathogenesis

A

Patients dont produce as many paneth cells
- means less defensins and increases in inflammatory pathogen presence

Eventually leads to ulcers in the GI tract/gut with chronic exposure to the pathogens

also is believed that the commensal bacteria also trigger an inappropriate mucosal immune response that is never enough to kill infectious bacteria, but is enough to chronic all damage intestinal tissues

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7
Q

What bacteria do defensins bind to?

A

Gram (+) bacteria
- binds to the carbohydrates of the peptidoglycan wall, poking holes in them (bacteriocidal)

is innate immunity

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8
Q

Peyer patches

A

Unencapsulated follicles of lymphoid tissues that is found in the lamina propria of the ilium and rectum primarily

Contains specialized M cells that sample and present antigens to immune cells
- if APC’s are present morphs resident dormant B-cells into secreting IgA plasma cells

*are the prime movers is innate defense in gut tissue *

IgA is produced due to production of TGF-B in the follicle when stimulated

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9
Q

M cells

A

Are the prime APC’s in the gut tissues

- take bacteria antigens and M-cells upregulated them and present them to T-cells/B-cells

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10
Q

TLR signaling in GALT tissue

A

A little bit different and results in 4 main functions:

1) produces factors that promote motility and repair epithelium
2) participates in promoting B-cell production of IgA
3) maintains tight junctions integrity
4) increase expression of defensins

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11
Q

Why are there no immune responses to the commensal bacteria present in GALT?

A

TLR’s are absent from the apical membrane (lumen surface) on the epithelial cells

  • TLR signaling only initiates if bacteria crosses the epithelial cells
  • also DC’s only are weakly activated by commensal bacteria so instead produces Tregs vs defensins
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12
Q

GALT adaptive immunity

A

Initiates when the antigens cross the internal mucosa

  • 2 ways this occurs*:
    1) transcytosis of antigens through M-cell’s -> Peyer’s patch

2) dendritic cells capture antigens and transport them to secondary lymphatic tissues by transporting between adjacent cells

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13
Q

What do Tcells release in result to both pathogenic and commensal bacteria?

A

Pathogenic = T-helper cells and CTL’s

Commensal = Tregs

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14
Q

Why is IgA the prime antibody in GI tract?

A

Because it is attached to a J-chain that allows it to bind to epithelial tissues and cross tight junctions
- only one that can do this

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15
Q

What are the typical GI microbiome bacteria?

A

Enterobacteria except for

  • campylobacter
  • vibrio
  • yersinia
  • shigella
  • salmonella

LOTS of gram (-) rods anaerobic bacteria

Streptococci

Staph aureus

Yeasts

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16
Q

Do male or female sex hormones produce a more inflammatory GI environment?

A

Females

- hence why females tend to get IBS/IBD easier

17
Q

What factors can affect GI microbiome

A

Genetics

Diet

Antibiotics
- should take probiotics with it

Metabolic disease

Autoimmunity Issues

Increased susceptibility

18
Q

What is fecal microbiome transplant (FMT)?

A

Transplant fecal matter from one person to another

Done in patients with autoimmune disorders, recurrent c. Diff infections and type 2 diabetes, etc.

19
Q

What 3 factors lead to autoimmunity in the gut?

A

Genetics

Environmental factors

Gut Dysbiosis

20
Q

What two disorders are included in IBD?

A

Crohn’s disease

Ulcerative colitis

21
Q

Difference between ulcerative colitis and Crohn’s disease

A

Ulcerative colitis

  • involves only colon and rectum
  • almost always produces bloody diarrhea
  • not much ab pain
  • NO fistula And perianal disease
  • “lead pipe” appearance on imaging with loss of haustra
  • deep ulcers with friable mucosa and crypt abscesses is always present.
  • continuous ulcer lesions are present
  • is TH2 mediated
  • associated with p-ANCA antibodies
  • smoking is actually protective

Crohn’s disease

  • involves any part of the GI tract EXCEPT rectum. Usually affects terminal ileum and colon though
  • presents with fistula and perianal disease
  • usually no bloody diarrhea and severe ab pain
  • shows aphthoid and deep ulcers with cobblestone mucosa and creeping fat pouches
  • “string sign” on affected portion with RLQ mass
  • tranmural lesions and crypt abscesses
  • smoking worsens condition
  • common associated with Anti-Saccharomyces antibodies (ASCA)
22
Q

Treatment for both Crohn’s disease and ulcerative colitis

A

Crohn’s:

  • corticosteroids
  • azathioprine (halts purine synthesis)
  • antibiotics or biological

Ulcerative colitis:

  • colonectomy
  • 5-aminosalicyclic
  • 6-mercaptopurine
23
Q

Most common symptoms of Crohn’s disease

A

Severe RLQ pain

Non-bloody diarrhea

Weight loss

24
Q

Most common symptoms of ulcerative colitis

A

Bloody diarrhea

Mild ab pain and cramping

(+/-) weight loss

25
Q

Irritable bowel syndrome

A

Essentially a lesser IBD

- hard to distinguish since symptoms are similar to IBD

26
Q

Probiotics

A

Helps recover good flora after diarrheal disease or antibiotic therapies

Essential for patients who have just had their microbiome wiped out, but doesnt really replace still intact microbiome

must ask patient to use probiotics (yogurt/supplements/etc) if they are on high dose or long term corticosteroids

also doesnt cure active infections or really help, more of a preventive measure

27
Q

What are prebiotics?

A

Fiber

- cleans out and creates healthy environment for microbiome to thrive

28
Q

Celiac disease

A

Is a type 4 delayed type of hypersensitivity towards Gliadin (gluten) and endomysium autoantigens

Results in lymphocytes and macrophages invading the jejunum every tine gliadin reaches the jejunum
- results in inflammation and diarrhea