Department of Microbiology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390, USA.
Department of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, One Shields Avenue, Davis, California 95616, USA.
Nature. 2018 Jan 11;553(7687):208-211. doi: 10.1038/nature25172. Epub 2018 Jan 3.
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.
胃肠道炎症性疾病常与菌群失调有关,其特征是肠道微生物群落发生变化,包括肠杆菌科(变形菌门)兼性厌氧菌的扩张。在这里,我们表明,通过钨酸盐处理可以预防肠道炎症期间肠杆菌科的失调性扩张,钨酸盐选择性抑制只有在炎症发作期间才起作用的钼辅因子依赖的微生物呼吸途径。相比之下,我们发现钨酸盐处理在稳态条件下对微生物组组成的变化很小。值得注意的是,钨酸盐介导的微生物组编辑可减轻结肠炎小鼠模型中肠道炎症的严重程度。我们的结论是,通过钨酸盐处理精确编辑微生物组组成可以改善炎症肠道中菌群失调的不良影响。