Helmholtz Gemeinschaft


Salt-responsive gut commensal modulates TH17 axis and disease

Item Type:Article
Title:Salt-responsive gut commensal modulates TH17 axis and disease
Creators Name:Wilck, N. and Matus, M.G. and Kearney, S.M. and Olesen, S.W. and Forslund, K. and Bartolomaeus, H. and Haase, S. and Maehler, A. and Balogh, A. and Marko, L. and Vvedenskaya, O. and Kleiner, F.H. and Tsvetkov, D. and Klug, L. and Costea, P.I. and Sunagawa, S. and Maier, L. and Rakova, N. and Schatz, V. and Neubert, P. and Fraetzer, C. and Krannich, A. and Gollasch, M. and Grohme, D.A. and Corte-Real, B.F. and Gerlach, R.G. and Basic, M. and Typas, A. and Wu, C. and Titze, J.M. and Jantsch, J. and Boschmann, M. and Dechend, R. and Kleinewietfeld, M. and Kempa, S. and Bork, P. and Linker, R.A. and Alm, E.J. and Mueller, D.N.
Abstract: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 (T(H)17) cells, which can also contribute to hypertension. Induction of T(H)17 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 T(H)17 cells. In line with these findings, a moderate high-salt challenge in a pilot study in humans reduced intestinal survival of Lactobacillus spp., increased T(H)17 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.
Keywords:Animals, Mice
Publisher:Nature Publishing Group (U.K.)
Page Range:585-589
Date:30 November 2017
Official Publication:https://doi.org/10.1038/nature24628
PubMed:View item in PubMed

Repository Staff Only: item control page

Open Access
MDC Library