New research, published in the journal Nature Immunology, now shows how a high intake of salt may cause inflammation in multiple sclerosis.
Multiple sclerosis (MS) is an autoimmune disorder in which the body’s immune system destroys the protective coating around neurons called myelin.
This neurological disease affects around
Generally, women are at a higher risk of developing the condition than men.
While researchers do not yet know what causes MS, an interplay between genetic predisposition and environmental factors is likely to be key.
For instance, researchers have so far identified 233 haplotypes that underpin MS. A haplotype is a set of genetic variants that can be found on the same chromosome and that is inherited from one parent.
As for environmental factors,
However, until now, the precise molecular mechanism behind this effect that salt has on MS was not known. New research finds a molecular pathway that explains how a high-salt environment might potentially trigger the autoimmune disorder.
Tomokazu Sumida, an associate research scientist in the Hafler laboratory at the Yale School of Medicine in New Haven, CT, is the first author of the
In their study, Sumida and colleagues analyzed regulatory T cells (Tregs) taken from people with MS. The main role of these cells is to control the immune response by regulating or suppressing other immune cells.
Tregs also “control the immune response to self and foreign particles (antigens) and help prevent autoimmune disease.”
As the researchers explain, the scientists identified this imbalance in people with MS and “in a high-salt environment.”
The researchers used RNA sequencing to analyze Tregs further, and they found that a protein called beta-catenin plays a key role in both keeping Tregs functional and regulating the two pro- and anti-inflammatory cytokines mentioned above.
The study also revealed that beta-catenin works together with a protein receptor called PTGER2 to trigger inflammation induced by a high salt intake. The authors conclude:
“Our findings suggest that the beta-catenin-PTGER2 axis serves as a bridge between environmental factors and autoimmune disease by modulating Treg function, and this axis may be involved in the pathogenesis of autoimmune disease.”
Asked about the clinical implications of his findings, Sumida told Medical News Today, “Not only upregulation of [the] pro-inflammatory cytokine IFN-gamma but also downregulation of [the] anti-inflammatory cytokine IL-10 might mark dysfunctional [Tregs] in MS patients.”
“Therefore,” he continues, “it would be ideal to work on [both directions]: prevent IFN-gamma and enhance IL-10, it’s always important to balance pro- and anti-inflammatory arms together.”
“Since this imbalance is enhanced under high salt environment, the people at risk of developing MS should consider lowering high salt intake.”
He added that the PTGER2-beta-catenin axis may be of interest to cancer researchers “because these two molecules are well-studied carcinogenic factors,” and it would be interesting to see if a high salt intake affects this axis in cancer, too.
“I would suggest to have [a] healthy diet with low salt content as an immunologist and also as a cardiologist,” he concluded.