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GI II > Immune-Pathogenic Mechanisms of IBD (Shnyra) > Flashcards

Immune-Pathogenic Mechanisms of IBD (Shnyra) Flashcards

1
Q

What disorders make up Inflammatory Bowel Disease

A

Chron’s Disease

Ulcerative Colitis

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2
Q

What are the major phases in the development of IBD

A
  1. Genetic and environmental factors induce impared barrier function
  2. Translocation of commensal bacteria which activate immune cells and cytokine production
  3. If an acute inflammation can’t be resolved it leads to chronic intestinal inflammation
  4. This can lead to complications such as fibrosis, stenosis, abscess, fistula, cancer, etc.
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3
Q

What are the characteristics of Chron’s Disease

Signs & Symptoms

GI involvement

Pathology

Diagnosis

Cancer Risk

Management & Treatment

Lab

A

Signs & Symptoms - Abdominal pain, obstruction & fever

GI involvement - Mouth to Anus (rectum spared)

Pathology - Abscesses, fistuals, strictures, granulomas, transmural inflammation

Diagnosis -“string sign” on barium x-ray, Skip lesions, Cobblestone appearance on endoscopy

Cancer Risk - Increased after 15 years

Management & Treatment - Medical surgery not curative

Lab - ASCA positive (80% of pts)

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4
Q

What are the characteristics of Chron’s Disease

Signs & Symptoms

GI involvement

Pathology

Diagnosis

Cancer Risk

Management & Treatment

Lab

A

Signs & Symptoms - Bloody diarrhea, Urgency

GI involvement - Colon and/or rectum

Pathology - Pseudopolyps, Toxic megacolon, Mucosal or submucosal inflammation

Diagnosis - Ulcerations, Edema, Erythema & erythema of colonic mucosa, Negative stool cultures, Continuos Disease

Cancer Risk - Increased after 10 yrs

Management & Treatment - Medical surgery can be curative

Lab - Positive pANCA

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5
Q

What factors have a major effect on Gut Microbiota

A

Diet

Environment

Genetics

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6
Q

What type of triggers are necessary to initiate or reactivate IBD

A

Environmental triggers

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7
Q

What areas does IBD typically develop

A

Areas of high bacterial concentrations

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8
Q

What major phyla contribute to the human microbiome

A

Firmicutes

Bacteroidetes

Actinobacteria

Proteobacteria

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9
Q

What are the major Phyla in:

Normal large intestine microbiome

Ulcerative Colitis

Chron’s Disease

A

Normal large intestine microbiome - Bacteroidetes & Firmicutes

Ulcerative Colitis - Proteobacteria > other phyla

Chron’s Disease - Firmicutes > Actinobacteria > Other phyla

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10
Q

The prevalence of IBD is inversely associated with the prevalence of what?

A

Helminth colonization

Helminths are thought to play an important immunoregulatory role with the intestinal flora

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11
Q

What is the main genetic predisposition for developing IBD

A

Single Nucleotide Polymorphisms (SNPs) - loci variants with alleles that differ at a single base

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12
Q

What SNP mutation found in chromosome 16 is associated with CD

A

IBD-1 mutation

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13
Q

What gene does IBD-1 locus contain

A

CARD15/NOD2 gene

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14
Q

What is the normal function of CARD15/NOD2 gene

A

A pattern recognition receptor expressed in macrophages and dendritic cells that recognizes MDP (a peptidoglycan found on bacteria) which triggers activation of NF-kB

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15
Q

How does mutations in CARD15/NOD2 contribute to CD

A

Defective function of macrophages ​

  • Leads to persistent intracellular infection of macrophages and chronic stimulation of T cells by macrophage-infecting organisms

Defective epithelial-cell responses

  • Lead to loss of barrier function and increased exposure to the mucosal microflora

Defective “conditioning” of APCs

  • Leads to inappropriate activation of APCs and disruption of the homeostatic balance of effector and regulator cells
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16
Q

List the role of commensal anti-inflammatory microflora in GI tract homeostasis

A
  1. Induce development of GALT
  2. Influences permeability and intestinal immunity
  3. Mantains basal levels of Th17 & Th1 cell activity in the lamina propria
  4. Suppression of pathobionts via induction of Treg cells and stimulation of IL-10 production by immune cells
  5. Ferment nondigestible polysaccharides to produce SCFAs which have anti-inflammatory properties in macrophages, DCs, CD4+ & intestinal epithelial cells.
17
Q

Colonization of the gut with segmented filamentous bacteria (SFB) results in what

A
  1. Induction of Treg cells in the lamina propria
  2. Maintenance of the basal activation level of Th17 cells which are important for the integrity of the epithelial barrier
18
Q

What consist of the mucosal firewall & what is the function

A

Combination of the epithelial barrier, mucus layer, IgA, DCs and T cells.

Limit the passage and exposure of commensals to the gut-associated lymphoid tissure, preventing untoward activation and pathology

19
Q

What is the relationship between immune tolerance & microbiota

A

Commensal microbiota suppress NF-KB pathway which promotes tolerance of DCs and macrophages to microflora and thus do not secrete pro-inflammatory cytokines. In IBD, tolerance is lost

20
Q

Chronic inflammation in IBD involves what

A

Hyperactivation of TH1 and TH17 cells

Inhitbion of Treg cells producing IL-10

21
Q

What is the pathogenesis of Chron’s disease

A
  1. Dendritic cells and macrophages secrete IL-12 which activate Th1 cells & secrete IL-6, IL-23 and TGF-B which activate Th17 cells
  2. Th1 cells secrete IL-2, INF-y and TNF while Th17 cells secrete IL-17
  3. These inflammatory cytokines lead to the development of Chron’s disease
22
Q

What is the pathogenesis of Ulcerative Colitis

A

An atypical activation of Th2 cells and NKT cells which produce the following cytokines:

Th2 –> IL-5, IL-4 & IL-13

NKT cells –> IL-13

23
Q

ROLE OF CYTOKINES IN IBD

A

Look at slide 52 and memorize it!

24
Q

What cytokines & substance promotes differentiation of T cells into T reg cells

A

Il-2 & TGF-B

Retinoic acid

25
Q
A
26
Q

What is the function of T reg cells

A

Secrete IL-10 & TGF-B leading to homeostasis of the GI microflora by supressing Th1, Th2 & Th17 cells

27
Q

What are current immuno-therapeutic approaches in treatment of IBD

A
  1. TNF blockers
  2. Fecal Microbiota Transplantation (FMT)
28
Q
A

GI II (3 decks)

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