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Induction and Clinical Scoring of Chronic-Relapsing Experimental Autoimmune Encephalomyelitis
Published on: July 4, 2007
A pain-mediated neural signal induces relapse in murine autoimmune encephalomyelitis, a multiple sclerosis model
Yasunobu Arima1, Daisuke Kamimura1, Toru Atsumi1
1Division of Molecular Neuroimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
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.
Insights
Pain can trigger relapse in experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis (MS). This study reveals how pain activates neural signals leading to inflammation and disease recurrence.
Area of Science:
- Neuroimmunology
- Immunology
- Pathogenesis of autoimmune diseases
Background:
- Pain is a common symptom in diseases like multiple sclerosis (MS), but its role in disease progression is unclear.
- Experimental autoimmune encephalomyelitis (EAE) serves as a model to study MS pathogenesis.
Purpose of the Study:
- To investigate the role of pain in inducing relapse of experimental autoimmune encephalomyelitis (EAE).
- To elucidate the underlying mechanisms by which pain influences disease relapse in EAE.
Main Methods:
- Utilized the murine EAE model to study pain-induced disease relapse.
- Performed mechanistic analysis involving sensory-sympathetic signaling, chemokine-mediated cell accumulation, and immune cell recruitment.
- Investigated antigen-presentation activity of specific immune cells in the spinal cord.
Main Results:
- Pain induction was shown to trigger EAE relapse in the EAE model.
- A sensory-sympathetic signal activates chemokine-mediated accumulation of antigen-presenting cells (MHC class II+CD11b+) at specific spinal cord vessels.
- This leads to the recruitment of pathogenic immune cells, including CD4+ T cells, resulting in EAE relapse.
Conclusions:
- Pain can initiate a neural signal that translates into an inflammatory response, specifically at certain blood vessels.
- This pain-induced inflammation can trigger disease relapse in EAE, suggesting a novel therapeutic target.
- Targeting the pain-mediated neural pathway offers a potential strategy for managing autoimmune disease relapse.
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