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Pathogenesis of Inflammatory Bowel Disease Poster

By AHayesOZ Feb 13, 2012 400 Words
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Genetic Susceptibility

• Different genetic abnormalities can lead to similar disease phenotypes. • Genes associated with Crohn's disease are not implicated in Ulcerative Colitis • There is similar chromosomal susceptibility in CD and UC.

Crohn’s diseaseUlcerative Colitis

Mutant CARD15 causes;
Decreased antimicrobial peptide secretions
from Paneth cells of the small intestine
Defective down-regulation of innate immune
response to bacterial adjuvants
Ineffective clearance of intra- cellular
bacteria infections Proliferation of luminal and mucosally
adherent commensal bacteria
Anti TNF (tumour necrosis factor) may
also cause inflammation

Immune Response

• Innate and acquired immune systems are activated
• Loss of tolerance to enteric commensal bacteria
• Cells of Innate immune system response are similarly activated • Proinflammatory cytokine and chemokine expression is upregulated • Expression of adhesion molecules and costimulatory molecules is increased

Crohn’s disease Ulcerative Colitis

• Enteric microflora stimulate
immune responses either by
functioning as adjuvants or antigens.
o Adjuvants activate innate immune responses, including dendritic cells and other APCs o Antigens stimulate the clonal expansion of T cells that selectively recognize the antigen through their T-cell receptor leading to aggravated T-cell response • There is both bacterial and host specificity to each disease

Crohn’s disease Ulcerative Colitis

Luminal Microbial Antigens and Adjuvants

• Infection and NSAIDS -Initiate non-specific inflammation and break mucosal barrier • Diet - Implicated by patients but mechanisms poorly understood • Aluminium and Iron may have adjuvant activity and stimulate bacterial virulence and dysbiosis • Stress - alters mucosal permeability and blood flow

• Smoking - Contributor to Crohn’s but preventative to Ulcerative Colitis.
• Appendectomy - Preventative against Ulcerative colitis

• Persistent pathological infection -
o Mycobacterium Avium Paratuberculosis – Contributor to Crohn’s o Enteroadherent and Invasive E. Coli - likely cause of Crohn’s

Environmental Triggers

Mucosal Barrier Integrity – Breaks more easily

Immunoregulation – Exaggerated response

Homeostasis of Pathogenic:Beneficial Enteric

Bacteria - Dysbiosis

Implicated genes regulate several biological functions that affect:

Weaker genetic link
No gene specifically linked
HLA factors (determine blood groups)
can predict behaviour of pathogenesis.

T-helper type 1 and 17 cytokine mediated process, with deficient innate immune response

An atypical T-Helper type 2 disorder showing natural killer cell and IL-13 activity

More strongly implicated to commensal

Increased numbers of enteric
Bacteroides s.p.p and
Enterobacteriaceae s.p.p shown
in infected areas

Persistent luminal antigen stimulation
is required for transfer of Colitis

Environmental triggers influence susceptibility to inflammation, increases uptake of commensal bacterial antigens and adjuvants and improves luminal microenvironment.

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