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

Authors :
Wilck N
Matus MG
Kearney SM
Olesen SW
Forslund K
Bartolomaeus H
Haase S
Mähler A
Balogh A
Markó L
Vvedenskaya O
Kleiner FH
Tsvetkov D
Klug L
Costea PI
Sunagawa S
Maier L
Rakova N
Schatz V
Neubert P
Frätzer C
Krannich A
Gollasch M
Grohme DA
Côrte-Real BF
Gerlach RG
Basic M
Typas A
Wu C
Titze JM
Jantsch J
Boschmann M
Dechend R
Kleinewietfeld M
Kempa S
Bork P
Linker RA
Alm EJ
Müller DN
Source :
Nature [Nature] 2017 Nov 30; Vol. 551 (7682), pp. 585-589. Date of Electronic Publication: 2017 Nov 15.
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 <subscript>H</subscript> 17) cells, which can also contribute to hypertension. Induction of T <subscript>H</subscript> 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 <subscript>H</subscript> 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 <subscript>H</subscript> 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.

Details

Language :
English
ISSN :
1476-4687
Volume :
551
Issue :
7682
Database :
MEDLINE
Journal :
Nature
Publication Type :
Academic Journal
Accession number :
29143823
Full Text :
https://doi.org/10.1038/nature24628