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BioMed Research International
Volume 2014 (2014), Article ID 675786, 9 pages
http://dx.doi.org/10.1155/2014/675786
Research Article

Monocolonization of Germ-Free Mice with Bacteroides fragilis Protects against Dextran Sulfate Sodium-Induced Acute Colitis

1Graduate Institute of Sports Science, National Taiwan Sport University, Taoyuan 333, Taiwan
2Department of Molecular Biology and Human Genetics, Tzu Chi University, Hualien 970, Taiwan
3Graduate Institute of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan
4National Applied Research Laboratories, National Laboratory Animal Center, Taipei 115, Taiwan
5Department of Microbiology, National Taiwan University College of Medicine, Taipei 115, Taiwan

Received 13 March 2014; Accepted 27 April 2014; Published 29 May 2014

Academic Editor: Sang Hoon Rhee

Copyright © 2014 Chien-Chao Chiu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Ulcerative colitis is inflammatory conditions of the colon caused by interplay of genetic and environmental factors. Previous studies indicated that the gut microflora may be involved in the colonic inflammation. Bacteroides fragilis (BF) is a Gram-negative anaerobe belonging to the colonic symbiotic. We aimed to investigate the protective role of BF in a colitis model induced in germ-free (GF) mice by dextran sulfate sodium (DSS). GF C57BL/6JNarl mice were colonized with BF for 28 days before acute colitis was induced by DSS. BF colonization significantly increased animal survival by 40%, with less reduction in colon length, and decreased infiltration of inflammatory cells (macrophages and neutrophils) in colon mucosa following challenge with DSS. In addition, BF could enhance the mRNA expression of anti-inflammatory-related cytokine such as interleukin 10 (IL-10) with polymorphism cytokine IL-17 and diminish that of proinflammatory-related tumor necrosis factor α with inducible nitric oxide synthase in the ulcerated colon. Myeloperoxidase activity was also decreased in BF-DSS mice. Taking these together, the BF colonization significantly ameliorated DSS-induced colitis by suppressing the activity of inflammatory-related molecules and inducing the production of anti-inflammatory cytokines. BF may play an important role in maintaining intestinal immune system homeostasis and regulate inflammatory responses.