Sodium chloride triggers Th17 mediated autoimmunity

Item Type:	Review
Title:	Sodium chloride triggers Th17 mediated autoimmunity
Creators Name:	Haase, S. and Wilck, N. and Kleinewietfeld, M. and Müller, D.N. and Linker, R.A.
Abstract:	The detrimental effects of a high-salt diet on human health have received much attention in the past few years. While it has been well established that high dietary salt intake is related to cardiovascular diseases, there is growing evidence that excess salt also affects the immune system and might be considered as a risk factor in autoimmune diseases such as multiple sclerosis (MS). Several studies have implicated T helper 17 cells (Th17) in the pathogenesis of MS. We and others recently demonstrated that excessive salt enhances the differentiation of Th17 cells, inducing a highly pathogenic phenotype that aggravates experimental neuroinflammation. Moreover, a diet rich in sodium affects intestinal microbiota alongside increased intestinal Th17 cells, thus linking the detrimental effects of high salt consumption to the gut-immune axis. First human studies revealed an association of increased MS disease activity with elevated sodium chloride consumption, while more recent epidemiology studies in larger cohorts suggest no correlation between salt intake and MS. However, it is known that ordinary urinary sodium analyses and nutritional questionnaires do not necessarily correspond to the actual sodium load and more sophisticated analyses are needed. Moreover, studies revealed that sodium can temporarily be stored in the body. This review summarizes recent findings on the impact of salt on the immune system and discusses potential challenges investigating dietary salt intake as a risk factor in MS.
Keywords:	Autoimmunity, Gastrointestinal Microbiome, Multiple Sclerosis, Sodium Chloride, Dietary, Th17 Cells, Animals
Source:	Journal of Neuroimmunology
ISSN:	0165-5728
Publisher:	Elsevier
Volume:	329
Page Range:	9-13
Date:	15 April 2019
Additional Information:	Copyright © 2018 Elsevier B.V. All rights reserved.
Official Publication:	https://doi.org/10.1016/j.jneuroim.2018.06.016
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