Role of diet and gut microbiota in multiple sclerosis: New findings on the role of high‐salt intake in induction of neuroinflammation

Abstract

Multiple etiological factors are involved in the pathogenesis of multiple sclerosis (MS). The recent study by Okuno et al. provides an insight into the interaction of gut microbiota and immune cells in MS. However, new findings showed that a high-salt diet is involved in the induction of severe neuroinflammation through the aggravation of T helper 17 pathways and their inflammatory cytokines. The synergistic effects of high-salt and high-fat intake in the induction of inflammatory reactions are also plausible. This article is a snapshot of the recent findings about the putative role of highsalt intake in the pathogenesis of MS.New findings on the role of high-salt intake in induction of neuroinflammation New findings revealed the interaction of gut microbiota and immune cells in MS. This topic was adeptly reviewed by Okuno et al. in a recent special issue of Clinical and Experimental Neuroimmunology. 1 As reviewed, the gut microbiota of MS patients has a distinct pattern in comparison with healthy individuals. 1 In animal models of MS (e.g. experimental autoimmune encephalomyelitis [EAE]), involvement of gut flora in augmentation of immune responses toward neural inflammation and autoantibody production has been observed as well. 1 In addition to these important findings, new investigations have shown the role of high-salt intake in the pathogenesis of MS through induction of severe neuroinflammation. 2 The first findings in this regard were published in two studies in 2013 in Nature, and showed that excessive salt intake augments the T helper 17 (T H 17) cells in the EAE mouse model. 3,4 The pathways involved in the induction of T H 17 cells after high-salt intake are related to activation of the p38/mitogen-activated protein kinase, nuclear factor of activated T cells and serum glucocorticoid-regulated kinase pathways (Table 1). [3][4][5][6][7] Notably, recent investigations showed that high-salt intake is involved in the induction of inflammatory reactions through disturbance of the gut microbiota (see recent reviews 2,8 ). In this regard, Wilck et al. found that a high-salt diet disturbs the murine gut microbiome and induces neuroinflammation through T H 17 expansion in the EAE-affected murine model. 9 Remarkably, neuroinflammation after high-salt exposure was related to disturbance of the mouse gut microbiome, especially depletion of Lactobacillus murinus. Conversely, recovery of L. murinus prohibited salt-induced neuropathology in the EAE model. 9 As such, in a pilot study in humans, high-salt intake diminished intestinal survival of Lactobacillus spp., and enhanced T H 17 cells and blood pressure. 9 Faraco et al. showed that high dietary salt induces neurovascular and cognitive dysfunction through a gut-initiated T H 17 responses. 10 Augmentation of these cells in the small intestine after a high-salt diet resulted in increased interleukin (IL)-17 concentration in the blood. These findings suggest a new gut-brain axis linking dietary salt intake. Although there is strong evidence regarding the pathogenesis...

Serum Untargeted Metabolism Reveals the Mechanism of L. plantarum ZDY2013 in Alleviating Kidney Injury Induced by High-Salt Diet

“…Research confirms the health risks of excessive salt intake, most notably the increased risk of cardiovascular disease associated with HSD [3]. Studies have also found that HSD can affect the body's immune system and may even increase the risk of autoimmune diseases [4,5]. In addition, HSD can increase the risk of gut related diseases and cancer, as well as affect the kidney system, skeletal system, and metabolic function [6,7].…”