Autor: |
Yasunobu Arima, Daisuke Kamimura, Toru Atsumi, Masaya Harada, Tadafumi Kawamoto, Naoki Nishikawa, Andrea Stofkova, Takuto Ohki, Kotaro Higuchi, Yuji Morimoto, Peter Wieghofer, Yuka Okada, Yuki Mori, Saburo Sakoda, Shizuya Saika, Yoshichika Yoshioka, Issei Komuro, Toshihide Yamashita, Toshio Hirano, Marco Prinz, Masaaki Murakami |
Jazyk: |
angličtina |
Rok vydání: |
2015 |
Předmět: |
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Zdroj: |
eLife, Vol 4 (2015) |
Druh dokumentu: |
article |
ISSN: |
2050-084X |
DOI: |
10.7554/eLife.08733 |
Popis: |
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. |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
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