Vasoactive intestinal polypeptide suppressed experimental autoimmune encephalomyelitis by inhibiting T helper 1 responses.

Vasoactive intestinal peptide (VIP) has been found to act as a potent anti-inflammatory factor through regulating the production of both anti- and pro-inflammatory mediators and promoting Th2-type responses. In this study, we used myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis (EAE) model in C57BL/6 mice to investigate the potential effects of VIP on multiple sclerosis. Our results showed that in vivo treatment of EAE-induced mice with VIP had great protective benefit at both clinical and histological levels. Disease suppression was associated with the inhibition of T cells proliferation, shifting of the immune response toward a Th2-type response and influencing the expression of pro-inflammatory cytokines including IFN-gamma, IL-6 and IL-2 as well as chemotactic factors such as RANTES. In conclusion, the study provides evidence that VIP had great protective effect on EAE through its inhibition actions on pathogenic T cells and through a specific effect on the Th1 response.