Departments of Immunology and Infectious Diseases and Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Beth Israel Deaconess Medical Center, Boston, MA 02215, USA.
Science. 2020 Sep 18;369(6510):1518-1524. doi: 10.1126/science.abb3763.
Associations between chronic kidney disease (CKD) and the gut microbiota have been postulated, yet questions remain about the underlying mechanisms. In humans, dietary protein increases gut bacterial production of hydrogen sulfide (HS), indole, and indoxyl sulfate. The latter are uremic toxins, and HS has diverse physiological functions, some of which are mediated by posttranslational modification. In a mouse model of CKD, we found that a high sulfur amino acid-containing diet resulted in posttranslationally modified microbial tryptophanase activity. This reduced uremic toxin-producing activity and ameliorated progression to CKD in the mice. Thus, diet can tune microbiota function to support healthy host physiology through posttranslational modification without altering microbial community composition.
已经有人提出，慢性肾脏病（CKD）与肠道微生物群之间存在关联，但关于潜在机制仍存在一些疑问。在人类中，饮食中的蛋白质会增加肠道细菌产生的硫化氢（HS）、吲哚和吲哚硫酸酯。后两者是尿毒症毒素，而 HS 具有多种生理功能，其中一些功能是通过翻译后修饰来介导的。在 CKD 的小鼠模型中，我们发现，含高硫氨基酸的饮食会导致翻译后修饰的微生物色氨酸酶活性。这降低了尿毒症毒素产生的活性，并改善了小鼠的 CKD 进展。因此，饮食可以通过翻译后修饰来调节微生物群的功能，以支持健康的宿主生理，而不改变微生物群落组成。
