Analyses in mice suggest that dietary salt increases blood pressure partly by affecting some of the microbes that inhabit the gut. The implications of this work for hypertension warrant further study in humans. See Article p.585 The role of the gut microbiota in human disease is becoming increasingly recognized. In this study, Dominik Muller and colleagues report that a diet high in salt alters the composition of the gut microbiota in mice, causing pronounced depletion of the commensal Lactobacillus murinus and reduced production of indole metabolites. Previous work has suggested that a high salt diet leads to the generation of pathogenic T helper 17 (TH17) cells, which have been linked to hypertension and autoimmunity. The authors show that treatment of mice on a high salt diet with L. murinus prevents salt-induced aggravation of actively induced autoimmune encephalomyelitis and salt-sensitive hypertension, through the suppression of TH17 cells. In a pilot study in a small number of humans, the authors also show that high-salt challenge induces an increase in blood pressure and TH17 cells, associated with a reduction in Lactobacillus in the gut. However, future work is required to determine whether the findings for mice are translatable to humans.

中文翻译：

---

微生物群：细菌处于高压状态

对小鼠的分析表明，饮食中的盐分会影响一些栖息在肠道中的微生物，从而导致血压升高。这项工作对高血压的影响值得在人类中进一步研究。参见文章第 585 页 肠道微生物群在人类疾病中的作用越来越得到认可。在这项研究中，Dominik Muller 及其同事报告说，高盐饮食会改变小鼠肠道微生物群的组成，导致共生鼠乳杆菌明显消耗，并减少吲哚代谢物的产生。先前的研究表明，高盐饮食会导致致病性 T 辅助 17 (TH17) 细胞的产生，这些细胞与高血压和自身免疫有关。作者表明，用 L. murinus 通过抑制 TH17 细胞来防止盐诱导的主动诱导的自身免疫性脑脊髓炎和盐敏感性高血压的恶化。在对少数人进行的一项初步研究中，作者还表明，高盐挑战会导致血压和 TH17 细胞升高，这与肠道中乳酸杆菌的减少有关。然而，需要未来的工作来确定小鼠的发现是否可以转化为人类。