A pain-mediated neural signal induces relapse in murine autoimmune encephalomyelitis, a multiple sclerosis model
20.07.2015
Arima Y, Kamimura D, Atsumi T, Harada M, Kawamoto T, Nishikawa N, Stofkova A, Ohki T, Higuchi K, Morimoto Y, Wieghofer P, Okada Y, Mori Y, Sakoda S, Saika S, Yoshioka Y, Komuro I, Yamashita T, Hirano T, Prinz M, Murakami M.
eLife 2015;4:e08733
Although pain is a common symptom of various diseases and disorders, its contribution to disease pathogenesis is not well understood. Here we show using murine experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis (MS), that pain induces EAE relapse. Mechanistic analysis showed that pain induction activates a sensory-sympathetic signal followed by a chemokine-mediated accumulation of MHC class II+CD11b+ cells that showed antigen-presentation activity at specific ventral vessels in the fifth lumbar cord of EAE-recovered mice. Our results demonstrate that a painmediated neural signal can be transformed into an inflammation reaction at specific vessels to induce disease relapse, thus making this signal a potential therapeutic target.
