Chiu Chien-Chao, Ching Yung-Hao, Wang Yu-Chih, Liu Ju-Yun, Li Yen-Peng, Huang Yen-Te, Chuang Hsiao-Li
Graduate Institute of Sports Science, National Taiwan Sport University, Taoyuan 333, Taiwan.
Department of Molecular Biology and Human Genetics, Tzu Chi University, Hualien 970, Taiwan.
Biomed Res Int. 2014;2014:675786. doi: 10.1155/2014/675786. Epub 2014 May 29.
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.
溃疡性结肠炎是由遗传和环境因素相互作用引起的结肠炎症性疾病。先前的研究表明，肠道微生物群可能参与结肠炎症。脆弱拟杆菌（BF）是一种属于结肠共生菌的革兰氏阴性厌氧菌。我们旨在研究BF在葡聚糖硫酸钠（DSS）诱导的无菌（GF）小鼠结肠炎模型中的保护作用。在通过DSS诱导急性结肠炎之前，将BF定殖于GF C57BL/6JNarl小鼠28天。BF定殖显著提高了动物存活率40%，结肠长度减少较少，并且在用DSS攻击后结肠黏膜中炎性细胞（巨噬细胞和中性粒细胞）的浸润减少。此外，BF可增强抗炎相关细胞因子如白细胞介素10（IL-10）的mRNA表达以及多态性细胞因子IL-17，并减少溃疡性结肠中促炎相关肿瘤坏死因子α与诱导型一氧化氮合酶的表达。BF-DSS小鼠的髓过氧化物酶活性也降低。综上所述，BF定殖通过抑制炎症相关分子的活性并诱导抗炎细胞因子的产生，显著改善了DSS诱导的结肠炎。BF可能在维持肠道免疫系统稳态和调节炎症反应中发挥重要作用。
