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

抄録

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.

収録刊行物

• eLife

  eLife 4 e08733-, 2015-08-11

  eLife Sciences Publications

詳細情報

• CRID: 1050845763950605184
• NII論文ID: 120005757989
• HANDLE: 2115/61910
• ISSN: 2050084X
• 本文言語コード: en
• 資料種別: journal article
• データソース種別:
  • IRDB
  • CiNii Articles