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Interplay of commensal and pathogenic bacteria, genetic mutations, and immunoregulatory defects in the pathogenesis of inflammatory bowel diseases
Author(s) -
Packey C. D.,
Sartor R. B.
Publication year - 2008
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/j.1365-2796.2008.01962.x
Subject(s) - pathogenesis , ulcerative colitis , immunology , immune system , inflammatory bowel disease , pathogenic bacteria , inflammation , inflammatory bowel diseases , intestinal permeability , medicine , bacteria , commensalism , dysbiosis , microbiology and biotechnology , disease , genetic predisposition , biology , gut flora , genetics , pathology
Enteric microbiota can contribute to Crohn’s disease and ulcerative colitis in several ways. Pathogenic or functionally altered commensal bacteria with increased mucosal adherence, invasion and intracellular persistence can activate pathogenic T cells and chronic intestinal inflammation. Compositional changes in intestinal microbiota can lead to decreased protective and increased aggressive species. Genetic polymorphisms resulting in increased mucosal permeability, decreased microbial killing, ineffective clearance of bacteria, biased TH1 and TH17 immune responses and loss of immunological tolerance are probably key contributors to IBD. Future therapies for these heterogeneous diseases should be individualized based on the patient‐specific subset.