文献类型：期刊文献

英文题名：Desulfovibrio-Hydrogen Sulfide Mediates Capsaicin-Induced Oxidative Stress and Gut Inflammation via TXNIP/NLRP3 Pathway

作者：Zhu, Liangliang[1];Feng, Xiangru[1];Lu, Xiaoxuan[1];Han, Geng[1];Zou, Jiaqi[1];Dong, Zhaoyang[1,2,3];Luo, Ting[1,2,3];Jin, Jiayang[1,2,3];Zhao, Mengyao[1,2,3];Ji, Xiaoguo[1,2,3];Zhao, Liming[1,2,3]

机构：[1]East China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai, Peoples R China;[2]East China Univ Sci & Technol, Shanghai Frontiers Sci Ctr Optogenet Tech Cell Met, Sch Pharm, Shanghai, Peoples R China;[3]Shanghai Collaborat Innovat Ctr Biomfg Technol, Shanghai, Peoples R China

年份：2026

外文期刊名：FOOD BIOENGINEERING

收录：EI(收录号：20260720053194);WOS:【ESCI(收录号:WOS:001684143000001)】；

基金：Natural Science Foundation of Shanghai, Grant/Award Number: 23ZR1415400; The Young Scientists Fund of the National Natural Science Foundation of China, Grant/Award Number: 32302102

语种：英文

外文关键词：capsaicin; Desulfovibrio; Faecalibacterium prausnitzii; gut inflammation; hydrogen sulfide

摘要：The intake of capsaicin can disrupt the gut microecology and impact health, yet its underlying mechanism is not fully elucidated. This study, by establishing capsaicin-induced human microbiota-associated (HMA) mouse models revealed the molecular mechanism by which capsaicin perturbs the gut microbiota and metabolites, leading to intestinal barrier dysfunction, inflammation, and oxidative stress. This study demonstrated that capsaicin intake significantly increased the abundance of Desulfovibrio and raised the level of hydrogen sulfide (H2S). Concurrently, the abundance of Faecalibacterium prausnitzii, which shared a symbiotic relationship with Desulfovibrio, also increased. These changes resulted in impaired intestinal barrier function, oxidative stress, and inflammation. Through microbe-colonization and chromate (an H2S inhibitor) intervention experiments, it was confirmed that H2S, the metabolite of Desulfovibrio, mediated oxidative stress and triggered capsaicin-induced gut inflammation by activating the Thioredoxin-interacting protein (TXNIP)/NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) pathway. This study elucidated the mechanism by which capsaicin impaired gut health via the Desulfovibrio-H2S-TXNIP/NLRP3 pathway. It also provided a new target for improving and preventing intestinal health problems caused by dietary capsaicin.