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// Zhan Zhang 1 , Xinyue Wu 1 , Shuyuan Cao 1 , Li Wang 1 , Di Wang 1 , Hui Yang 1 , Yiming Feng 1 , Shoulin Wang 2 and Lei Li 1 1 Department of Hygiene Analysis and Detection, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, P. R. China 2 Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing, P. R. China Correspondence to: Lei Li, email: // Keywords : ulcerative colitis, caffeic acid, dextran sulfate sodium, NF-κB pathway, fecal microbiota, Immunology and Microbiology Section, Immune response, Immunity Received : March 25, 2016 Accepted : May 05, 2016 Published : May 11, 2016 Abstract Emerging evidence shows that dietary agents and phytochemicals contribute to the prevention and treatment of ulcerative colitis (UC). We first reported the effects of dietary caffeic acid (CaA) on murine experimental colitis and on fecal microbiota. Colitis was induced in C57BL/6 mice by administration of 2.5% dextran sulfate sodium (DSS). Mice were fed a control diet or diet with CaA (1 mM). Our results showed that dietary CaA exerted anti-inflammatory effects in DSS colitis mice. Moreover, CaA could significantly suppress the secretion of IL-6, TNFα, and IFNγ and the colonic infiltration of CD3 + T cells, CD177 + neutrophils and F4/80 + macrophages via inhibition of the activation of NF-κB signaling pathway. Analysis of fecal microbiota showed that CaA could restore the reduction of richness and inhibit the increase of the ratio of Firmicute to Bacteroidetes in DSS colitis mice. And CaA could dramatically increase the proportion of the mucin-degrading bacterium Akkermansia in DSS colitis mice . Thus, CaA could ameliorate colonic pathology and inflammation in DSS colitis mice, and it might be associated with a proportional increase in Akkermansia .
Zhang et al. (Wed,) studied this question.