Breaking the Cycle: Can Vitamin D Bridge the Gap Between Gut Microbiota and Immune Dynamics in Multiple Sclerosis?

Multiple Sclerosis (MS) is a chronic disease with autoimmune and neurodegenerative features that affect the nervous system. Genetic predisposition and environmental factors, such as vitamin D deficiency and dysbiosis activating a pro-inflammatory response, have a role in the etiology of the disease. In this context, the interactions of vitamin D with the gut microbiota and immune system have attracted attention in recent years. Vitamin D (1,25-dihydroxycholecalciferol) modulates the immune response by binding to the Vitamin D receptor (VDR). This pathway supports the functions of regulatory T cells by suppressing the activity of T helper cells 1 and 17 (Th1 and Th17). In MS patients, dysbiosis is characterized by a decrease in microbial diversity, and an increase in pro-inflammatory species is observed when compared to healthy individuals. Vitamin D has protective effects on eubiosis via VDR in intestinal epithelial cells, also reducing intestinal permeability by regulating tight junction proteins. In this way, vitamin D may contribute to the prevention of systemic inflammation. Although the relationship between vitamin D and the immune system is well documented, studies that address the triad of vitamin D level, gut microbiota, and immune response in MS are still limited.