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Salt-responsive gut commensal modulates TH17 axis and disease

Authors :
Wilck, Nicola
Matus, Mariana G.
Kearney, Sean M.
Olesen, Scott W.
Forslund, Kristoffer
Bartolomaeus, Hendrik
Haase, Stefanie
Mhler, Anja
Balogh, Andrs
Mark, Lajos
Vvedenskaya, Olga
Kleiner, Friedrich H.
Tsvetkov, Dmitry
Klug, Lars
Costea, Paul I.
Sunagawa, Shinichi
Maier, Lisa
Rakova, Natalia
Schatz, Valentin
Neubert, Patrick
Frtzer, Christian
Krannich, Alexander
Gollasch, Maik
Grohme, Diana A.
Crte-Real, Beatriz F.
Gerlach, Roman G.
Basic, Marijana
Typas, Athanasios
Wu, Chuan
Titze, Jens M.
Jantsch, Jonathan
Boschmann, Michael
Dechend, Ralf
Kleinewietfeld, Markus
Kempa, Stefan
Bork, Peer
Linker, Ralf A.
Alm, Eric J.
Mller, Dominik N.
Source :
Nature. November 30, 2017, Vol. 551 Issue 7682, p585, 5 p.
Publication Year :
2017

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[sub.H]17) cells, which can also contribute to hypertension. Induction of T[sub.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[sub.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[sub.H]17 cells and increased blood pressure. Our results connect high salt intake to the gutimmune axis and highlight the gut microbiome as a potential therapeutic target to counteract salt-sensitive conditions.<br />Author(s): Nicola Wilck [1, 2, 3, 4, 5]; Mariana G. Matus [6, 7]; Sean M. Kearney [6]; Scott W. Olesen [6]; Kristoffer Forslund [8]; Hendrik Bartolomaeus [1, 2, 3, 4]; [...]

Details

Language :
English
ISSN :
00280836
Volume :
551
Issue :
7682
Database :
Gale General OneFile
Journal :
Nature
Publication Type :
Academic Journal
Accession number :
edsgcl.516460250
Full Text :
https://doi.org/10.1038/nature24628