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Salt-responsive gut commensal modulates T(H)17 axis and disease

Item Type:Article
Title:Salt-responsive gut commensal modulates T(H)17 axis and disease
Creators Name:Wilck, N., Matus, M.G., Kearney, S.M., Olesen, S.W., Forslund, K., Bartolomaeus, H., Haase, S., Mähler, A., Balogh, A., Markó, L., Vvedenskaya, O., Kleiner, F.H., Tsvetkov, D., Klug, L., Costea, P.I., Sunagawa, S., Maier, L., Rakova, N., Schatz, V., Neubert, P., Frätzer, C., Krannich, A., Gollasch, M., Grohme, D.A., Côrte-Real, B.F., Gerlach, R.G., Basic, M., Typas, A., Wu, C., Titze, J.M., Jantsch, J., Boschmann, M., Dechend, R., Kleinewietfeld, M., Kempa, S., Bork, P., Linker, R.A., Alm, E.J. and Müller, 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:Animal Disease Models, Autoimmunity, Blood Pressure, Experimental Autoimmune Encephalomyelitis, Feces, Gastrointestinal Microbiome, Hypertension, Indoleacetic Acids, Indoles, Intestines, Lactobacillus, Lymphocyte Activation, Lymphocyte Count, Pilot Projects, Sodium Chloride, Symbiosis, Th17 Cells, Tryptophan, Animals, Mice
Publisher:Nature Publishing Group
Page Range:585-589
Date:30 November 2017
Official Publication:https://doi.org/10.1038/nature24628
External Fulltext:View full text on PubMed Central Europe
PubMed:View item in PubMed

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