Journal Article A pain-mediated neural signal induces relapse in murine autoimmune encephalomyelitis, a multiple sclerosis model

Arima, Yasunobu  ,  Kamimura, Daisuke  ,  Atsumi, Toru  ,  Harada, Masaya  ,  Kawamoto, Tadafumi  ,  Nishikawa, Naoki  ,  Stofkova, Andrea  ,  Ohki, Takuto  ,  Higuchi, Kotaro  ,  Morimoto, Yuji  ,  Wieghofer, Peter  ,  Okada, Yuka  ,  Mori, Yuki  ,  Sakoda, Saburo  ,  Saika, Shizuya  ,  Yoshioka, Yoshichika  ,  Komuro, Issei  ,  Yamashita, Toshihide  ,  Hirano, Toshio  ,  Prinz, Marco  ,  Murakami, Masaaki

4p.e08733 , 2015-08-11 , eLife Sciences Publications
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. Following this accumulation, various immune cells including pathogenic CD4+ T cells recruited in the spinal cord in a manner dependent on a local chemokine inducer in endothelial cells, resulting in EAE relapse. Our results demonstrate that a pain-mediated neural signal can be transformed into an inflammation reaction at specific vessels to induce disease relapse, thus making this signal a potential therapeutic target.

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