<i>Blautia producta</i> displays potential probiotic properties against dextran sulfate sodium-induced colitis in mice
Bingyong Mao, Weiling Guo, Shumao Cui, Qiuxiang Zhang, Jianxin Zhao, Xin Tang, Hao Zhang
Abstract
<i>Blautia</i> has attracted attention because of its potential efficacy in ameliorating host energy metabolism and inflammation. This study aims to investigate the influences of <i>Blautia</i> <i>producta</i> D4 on colitis induced by dextran sulfate sodium (DSS) and to reveal the underlying mechanisms. Results showed that <i>B. producta</i> D4 intervention significantly relieved body weight loss, and suppressed the elevation of pro-inflammatory cytokines [including interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β)] and excessive oxidative stress [myeloperoxidease (MPO) activity, superoxide dismutase (SOD) activity, glutathione peroxidase (GSH-Px) activity, and malondialdehyde (MDA) level] in colitis mice. Moreover, the concentrations of tight junction proteins (occludin, claudin-1, and ZO-1) related to the intestinal barrier were obviously elevated, and colitis-related TLR4/NF-κB pathway activation was remarkably inhibited after <i>B. producta</i> D4 intervention. The intestinal microbial disorder was evidently ameliorated by increasing the relative abundance of <i>Clostridium</i> <i>sensu</i> <i>stricto</i> 1, <i>Bifidobacterium</i>, GCA-900066225, <i>Enterorhabdus</i>, and reducing the relative abundance of <i>Lachnospiraceae</i> NK4A136 group. In conclusion, oral administration of <i>B. producta</i> D4 could ameliorate DSS-induced colitis by suppressing inflammatory responses, maintaining the intestinal barrier, inhibiting TLR4/ NF-κB pathway, and regulating intestinal microbiota balance. These results are conducive to accelerate the development of <i>B. producta</i> D4 as a functional probiotic for colitis.