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.
journal_name
Elifejournal_title
eLifeauthors
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 Mdoi
10.7554/eLife.08733subject
Has Abstractpub_date
2015-08-11 00:00:00issn
2050-084Xjournal_volume
4pub_type
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