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.
Others people have given TRPV1 agonists, which cause the painful sensation of chilli peppers and they have inhibited EAE in a number of studies (presumably because of the stress they cause). There is a suggestion that animals lacking animals TRPV1 and may not respond noxious stimuli don’t get EAE, we had no problem at all.
What is the next question? Does amputation of toes induce a relapse? Let’s not go there.
If this study is true then it implies relapsing EAE is due to pain signals an makes the ethics of doing such experiments more difficult. We and the Home Office have looked for pain faces (expresssions indicative of the presence of acute pain) of mice with EAE and they were not present.
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