Exopolysaccharides Produced by Bifidobacterium longum subsp. longum YS108R Ameliorates DSS-Induced Ulcerative Colitis in Mice by Improving the Gut Barrier and Regulating the Gut Microbiota

长双歧杆菌 微生物学 丁酸盐 肠道菌群 双歧杆菌 丁酸梭菌 溃疡性结肠炎 结肠炎 氧化应激 脂多糖 细菌 生物 炎症性肠病 化学 乳酸菌 发酵 食品科学 免疫学 生物化学 医学 疾病 遗传学 病理
作者
Huizhen Li,Huizhen Li,Haitao Li,Haitao Li,Catherine Stanton,R. Paul Ross,Jianxin Zhao,Wei Chen,Bo Yang
出处
期刊:Journal of Agricultural and Food Chemistry [American Chemical Society]
卷期号:72 (13): 7055-7073 被引量:20
标识
DOI:10.1021/acs.jafc.3c06421
摘要

Ulcerative colitis (UC) is a major disease that has endangered human health. Our previous study demonstrated that Bifidobacterium longum subsp. longum YS108R, a ropy exopolysaccharide (EPS)-producing bacterium, could alleviate UC in mice, but it is unclear whether EPS is the key substance responsible for its action. In this study, we proposed to investigate the remitting effect of EPS from B. longum subsp. longum YS108R on UC in a DSS-induced UC mouse model. Water extraction and alcohol precipitation were applied to extract EPS from the supernatant of B. longum subsp. longum YS108R culture. Then the animal trial was performed, and the results indicated that YS108R EPS ameliorated colonic pathological damage and the intestinal barrier. YS108R EPS suppressed inflammation via NF-κB signaling pathway inhibition and attenuated oxidative stress via the Nrf2 signaling pathway activation. Remarkably, YS108R EPS regulated gut microbiota, as evidenced by an increase in short-chain fatty acid (SCFA)-producing bacteria and a decline in Gram-negative bacteria, resulting in an increase of propionate and butyrate and a reduction of lipopolysaccharide (LPS). Collectively, YS108R EPS manipulated the intestinal microbiota and its metabolites, which further improved the intestinal barrier and inhibited inflammation and oxidative stress, thereby alleviating UC.
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