For those genetically susceptible to multiple sclerosis (MS), a diet high in sodium may be an environmental risk factor for the disease.
The findings, published in the Journal of the Federation of American Societies for Experimental Biology, better define how certain environmental risk factors influence the development of MS in those with a genetic risk. Previous studies in both humans and animals have shown that high levels of sodium augment the generation of T helper 17 cells, exacerbating autoimmune encephalomyelitis (EAE).
In the study, researchers induced EAE in three different genetic groups of mice and fed them either diets high in sodium or control diets with normal levels of sodium. In the C57BL6/J group, exposure to a high-sodium diet exacerbated EAE in both male and female mice, while a high sodium diet only exacerbated EAE in female mice in the SJL/JCrHsd group. They also found that sodium levels failed to affect EAE course in a third group: C57BL6/J mice carrying a 129/Sv-derived interval on chromosome 17. High levels of sodium did not seem to affect Th17 or Th1 responses, however it did weaken the blood-brain barrier and affect brain pathology — both of which are hallmarks of MS.
The study ultimately demonstrated that neuroinflammation related to MS is correlated to sex and genetics and mediated by the central nervous system.
Multiple sclerosis (MS) is a debilitating autoimmune neuroinflammatory disease influenced by genetics and the environment. MS incidence in female subjects has approximately tripled in the last century, suggesting a sex-specific environmental influence.
Recent animal and human studies have implicated dietary sodium as a risk factor in MS, whereby high sodium augmented the generation of T helper (Th) 17 cells and exacerbated experimental autoimmune encephalomyelitis (EAE), the principal model of MS. However, whether dietary sodium interacts with sex or genetics remains unknown.
Here, we show that high dietary sodium exacerbates EAE in a strain- and sex-specific fashion.