4.5 Article

Probiotic therapy in the prevention of pouchitis onset:: Decreased interleukin-1β, interleukin-8, and interferon-γ gene expression

Journal

INFLAMMATORY BOWEL DISEASES
Volume 11, Issue 5, Pages 447-454

Publisher

OXFORD UNIV PRESS INC
DOI: 10.1097/01.mpa.0000160302.40931.7b

Keywords

cytokines; gene expression; immunohistochemistry; pouchitis; probiotic therapy

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Background: Probiotic therapy has been shown to prevent the onset of pouchitis and to improve the quality of life in ulcerative colitis patients who required ileal pouch anal anastomosis. Pouchitis has been associated with elevated levels of proinflammatory cytokines and chemokines. Methods: In this retrospective analysis of archived endoscopic samples front responding patients enrolled in the above-mentioned trial, we were interested in Studying mucosal gene expression of the pleiotropic proinflammatory cytokines (interleukin-1 beta, interleukin-6), T(H)1 cytokines (interferon-gamma, tummor necrosis factor-alpha, interleukin-12) regulatory cytokines (interleukin-10, transforming growth factor-beta), and the chemokine interleukin-8. In addition to assessment of cytokine gene expression, the presence of polymorphonuclear cells in the mucosal tissue was evaluated. Results: Data show that patients who were treated with probiotics had significant lower mucosal mRNA expression levels of interleukin-10, interleukin-8, and interferon-gamma compared with placebo-treated patients. In addition, a lower number of polymorphonuclear cells was present in the tissue of patients within the probiotic group compared with the number of polymorphonulclear cells in the tissue of patients receiving placebo and patients having an episode of pouchitis. Conclusions: These data Suggest that probiotic treatment regulates the mucosal immune response by reducing mucosal levels of neutrophil-chemoattractant IL-8 and tissue influx of polymorphonuclear cells, and may further act by inhibition of T-cell activation, by reinforcement of barrier function and by a tight control of the potent pro-inflammatory cytokine IL-1 beta.

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