失调
结肠炎
微生物学
肠道菌群
炎症
肠杆菌科
蛋白质细菌
钨酸盐
生物
免疫学
细菌
化学
生物化学
大肠杆菌
遗传学
16S核糖体RNA
有机化学
基因
作者
Wenhan Zhu,Maria G. Winter,Mariana X. Byndloss,Luisella Spiga,Breck A. Duerkop,Elizabeth R. Hughes,Lisa Büttner,Everton de Lima Romão,Cassie L. Behrendt,Christopher A. Lopez,Luis Sifuentes-Dominguez,Kayci Huff-Hardy,Ronald P. Wilson,Caroline C. Gillis,Çağla Tükel,Andrew Y. Koh,Ezra Burstein,Lora V. Hooper,Andreas J. Bäumler,Sebastian Winter
出处
期刊:Nature
[Nature Portfolio]
日期:2018-01-01
卷期号:553 (7687): 208-211
被引量:395
摘要
Inflammatory diseases of the gastrointestinal tract are frequently associated with dysbiosis, characterized by changes in gut microbial communities that include an expansion of facultative anaerobic bacteria of the Enterobacteriaceae family (phylum Proteobacteria). Here we show that a dysbiotic expansion of Enterobacteriaceae during gut inflammation could be prevented by tungstate treatment, which selectively inhibited molybdenum-cofactor-dependent microbial respiratory pathways that are operational only during episodes of inflammation. By contrast, we found that tungstate treatment caused minimal changes in the microbiota composition under homeostatic conditions. Notably, tungstate-mediated microbiota editing reduced the severity of intestinal inflammation in mouse models of colitis. We conclude that precision editing of the microbiota composition by tungstate treatment ameliorates the adverse effects of dysbiosis in the inflamed gut.
科研通智能强力驱动
Strongly Powered by AbleSci AI