alexa Bifidobacterium Longum Alleviates Dextran Sulfate Sodium-induced Colitis By Suppressing IL-17A Response: Involvement Of Intestinal Epithelial Co-stimulatory Molecules | 21318
ISSN: 2329-8901

Journal of Probiotics & Health
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Junki Miyamoto, Eiji Miyauchi, Takuya Suzuki, Hiroshi Ohno and Soichi Tanabe
Posters: J Prob Health
DOI: 10.4172/2329-8901.S1.017
Abstract
Although some bacterial strains show potential to prevent colitis, their mechanisms are not fully understood. Here, we investigated the anti-colitic mechanisms of Bifidobacterium longum subsp. infantis JCM 1222T, focusing on the relationship between interleukin (IL)-17A secreting CD4+ T cells and intestinal epithelial co-stimulatory molecules in mice. Oral administration of JCM 1222T to mice alleviated dextran sulfate sodium (DSS)-induced acute colitis. The expression of type 1 helper T (Th1)- and IL-17 producing helper T (Th17)-specific cytokines and transcriptional factors was suppressed by JCM 1222T treatment. Intestinal epithelial cells (IECs) from colitic mice induced IL-17A production from CD4+ T cells in a cell-cell contact-dependent manner, and this was suppressed by oral treatment with JCM 1222T. Using blocking antibodies for co-stimulatory molecules, we revealed that epithelial co-stimulatory molecules including CD80 and CD40, which were highly expressed in IECs from colitic mice, were involved in IEC-induced IL-17A response. Treatment of mice and intestinal epithelial cell line Colon-26 cells with JCM 1222T decreased the expression of CD80 and CD40. Collectively, these data indicate that JCM 1222T negatively regulate epithelial co-stimulatory molecules, and this effect might be attributed, at least in part, to suppression of IL-17A in DSS-induced colitis.
Biography
Junki Miyamoto is a PhD student of Hiroshima University.
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