Bifidobacterium bifidum Ameliorates DSS-Induced Colitis in Mice by Regulating AHR/NRF2/NLRP3 Inflammasome Pathways through Indole-3-lactic Acid Production

被引:54
作者
Cui, Qingyu [2 ]
Zhang, Zhe [2 ]
Tian, Xiaoying [2 ]
Liang, Xi [2 ]
Lu, Youyou [2 ]
Shi, Yixin [2 ]
Kuerman, Malina [2 ]
Wang, Rui [2 ]
Zhou, Yu [2 ]
Gong, Pimin [2 ]
Lin, Kai [2 ]
Yi, Huaxi [2 ]
Li, Jiadong [1 ]
Liu, Tongjie [2 ]
Zhang, Lanwei [2 ]
机构
[1] China Innovat Probiot Sci Biotech Shanghai Co Ltd, R&D Ctr, Shanghai 200000, Peoples R China
[2] Ocean Univ China, Coll Food Sci & Engn, Qingdao 266100, Peoples R China
关键词
Bifidobacterium bifidum; ulcerative colitis; aryl hydrocarbon receptor; indole-3-lactic acid; probiotics; ARYL-HYDROCARBON RECEPTOR; GUT MICROBIOTA; BARRIER FUNCTION; TRYPTOPHAN; ACTIVATION; PROBIOTICS;
D O I
10.1021/acs.jafc.2c06894
中图分类号
S [农业科学];
学科分类号
09 ;
摘要
In this study, the effectors and mechanisms of Bifidobacterium bifidum FL-276.1 and B. bifidum FL-228.1 in alleviating dextran sulfate sodium (DSS)-induced colitis were investigated. Both FL-276.1 and FL-228.1 significantly alleviated DSS-induced colitis, whether they were supplemented from the beginning of the experiment (whole course intervention) or after the DSS induction started (partial intervention). Aryl hydrocarbon receptor (AHR) and the nuclear factor erythroid 2-related factor 2 (NRF2) pathways were activated in mice colons, while the NLR family pyrin domain containing 3 (NLRP3) was downregulated under the whole course intervention modes. Indole-3-lactic acid, an AHR ligand produced by FL-276.1 and FL-228.1, could regulate the AHR/NRF2/NLRP3 pathway in Caco-2 monolayers, thus upregulating the tight junction proteins and protecting the integrity of the epithelial barrier. These results are conducive to promoting clinical trials and product development of probiotics for alleviating colitis.
引用
收藏
页码:1970 / 1981
页数:12
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