A Western lifestyle with high salt consumption can lead to hypertension and cardiovascular disease. High salt may additionally drive autoimmunity by inducing T helper 17 (TH17) cells, which can also contribute to hypertension. Induction of TH17 cells depends on gut microbiota; however, the effect of salt on the gut microbiome is unknown. Here we show that high salt intake affects the gut microbiome in mice, particularly by depleting Lactobacillus murinus. Consequently, treatment of mice with L. murinus prevented salt-induced aggravation of actively induced experimental autoimmune encephalomyelitis and salt-sensitive hypertension by modulating TH17 cells. In line with these findings, a moderate high-salt challenge in a pilot study in humans reduced intestinal survival of Lactobacillus spp., increased TH17 cells and increased blood pressure. Our results connect high salt intake to the gut–immune axis and highlight the gut microbiome as a potential therapeutic target to counteract salt-sensitive conditions.

中文翻译：

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盐反应性肠道共生菌调节 TH17 轴和疾病


高盐摄入的西方生活方式会导致高血压和心血管疾病。高盐还可能通过诱导辅助 T 17 (TH17) 细胞来驱动自身免疫，这也可能导致高血压。 TH17 细胞的诱导取决于肠道微生物群；然而，盐对肠道微生物群的影响尚不清楚。在这里，我们发现高盐摄入量会影响小鼠的肠道微生物群，特别是通过消耗鼠乳杆菌。因此，用 L. murinus 治疗小鼠，通过调节 TH17 细胞，可以防止盐诱导的主动诱发的实验性自身免疫性脑脊髓炎和盐敏感性高血压的恶化。与这些发现一致的是，在一项针对人类的初步研究中，适度的高盐挑战会降低肠道中乳酸菌的存活率，增加 TH17 细胞的数量并导致血压升高。我们的研究结果将高盐摄入量与肠道免疫轴联系起来，并强调肠道微生物组是对抗盐敏感病症的潜在治疗靶点。