Any beneficial effects of mycobacteria on multiple sclerosis and experimental autoimmune encephalitis may include stimulation of the sympathetic nervous system

SummaryThe inhibitory effects of mycobacterial infection and mycobacterium components on multiple sclerosis (MS) and experimental autoimmune encephalitis (EAE; an animal model for MS) have been known for years. However, this effect seems like a paradox that both mycobacterial infection and MS induce type I immune responses. Some mechanisms have been proposed or even proven for this effect in different studies, but among them there is no hint of a possible role for the nervous system (NS). Regarding the close relations between sympathetic nervous system (SNS) and MS disease course, it can be hypothesized that SNS may have a role in the effects of mycobacterium on MS. Hypothesis: SNS can be stimulated by pro-inflammatory cytokines such as TNF-α and IL1-β, production of which are induced by mycobacterial infection or mycobacterium components. Although these cytokines can inhibit SNS in the site of inflammation caused by mycobacterium, they increase sympathetic tone in other places. The beneficial role of SNS in inhibiting or attenuating the course of MS and EAE has been suggested. Inhibitory effects of stimulated SNS on MS may occur via different ways such as inhibiting the production of pro-inflammatory cytokines and inducing the synthesis of anti-inflammatory cytokines, in other words, shifting the immune responses from type 1 toward type 2, as well as, induction of suppressor/regulator T lymphocytes, induction of heat shock proteins in brain and increasing the expression of Fas and Fas-ligand. Therefore, it seems that stimulation of SNS by mycobacterial infection or mycobacterium components is a key step in the mechanism of beneficial effects of mycobacterium on MS.