HUSCAP logo Hokkaido Univ. logo

Hokkaido University Collection of Scholarly and Academic Papers >
Institute for Genetic Medicine >
Peer-reviewed Journal Articles, etc >

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

Creative Commons License

Files in This Item:
e08733-download.pdf3.89 MBPDFView/Open
elife08733-figures.pdfFigures and figure supplements4.89 MBPDFView/Open
Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/61910

Title: A pain-mediated neural signal induces relapse in murine autoimmune encephalomyelitis, a multiple sclerosis model
Authors: Arima, Yasunobu Browse this author
Kamimura, Daisuke Browse this author →KAKEN DB
Atsumi, Toru Browse this author
Harada, Masaya Browse this author
Kawamoto, Tadafumi Browse this author →KAKEN DB
Nishikawa, Naoki Browse this author
Stofkova, Andrea Browse this author
Ohki, Takuto Browse this author
Higuchi, Kotaro Browse this author
Morimoto, Yuji Browse this author →KAKEN DB
Wieghofer, Peter Browse this author
Okada, Yuka Browse this author →KAKEN DB
Mori, Yuki Browse this author →KAKEN DB
Sakoda, Saburo Browse this author →KAKEN DB
Saika, Shizuya Browse this author →KAKEN DB
Yoshioka, Yoshichika Browse this author →KAKEN DB
Komuro, Issei Browse this author →KAKEN DB
Yamashita, Toshihide Browse this author →KAKEN DB
Hirano, Toshio Browse this author →KAKEN DB
Prinz, Marco Browse this author
Murakami, Masaaki Browse this author →KAKEN DB
Issue Date: 11-Aug-2015
Publisher: eLife Sciences Publications
Journal Title: eLife
Volume: 4
Start Page: e08733
Publisher DOI: 10.7554/eLife.08733
Abstract: 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.
Rights: http://creativecommons.org/licenses/by/4.0/
Type: article
URI: http://hdl.handle.net/2115/61910
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 村上 正晃

Export metadata:

OAI-PMH ( junii2 , jpcoar )

MathJax is now OFF:


 

Feedback - Hokkaido University