Methyl acetate arrests Th1 in peripheral immune system and alleviates CNS inflammation in EAE.

Multiple sclerosis (MS) is an inflammatory autoimmune disease of the central nervous system (CNS) mediated by immune cells. The pathogenesis of most autoimmune diseases has some degree of similarity to that of MS, and therefore the study of MS has clinical and scientific significance for other autoimmune diseases as well. As a widely used organic solvent, Methyl Acetate (MA) has a similar structure to acetate which has been shown to be therapeutic in the mouse model of multiple sclerosis. Here we found that MA was effective in reducing the disease severity of Experimental Autoimmune Encephalomyelitis (EAE). Pathological sections showed that MA reduced inflammatory cell infiltration in the CNS and attenuated demyelination in the spinal cord. MA increases the proportion of Th1 cells in the periphery of EAE mice. Further mechanistic studies have demonstrated that MA treatment induces Th1 retention in the peripheral immune system by increasing the expression levels of peripheral Th1-related chemokines CXCR3. CXCL9, CXCL10. In addition, we observed that MA alleviated intestinal inflammation in EAE mice. The data showed that this phenomenon is achieved by enhancing IL-10 and inhibiting IL-6 secretion. Our data indicates that MA might have therapeutic implications for autoimmune diseases such as MS.