Tonic Meningeal Interleukin-10 Upregulates Delta Opioid Receptor to Prevent Relapse to Pain
Inyang, K. E.; Sim, J.; Clark, K. B.; Matan, G.; Monahan, K.; Evans, C.; Beng, P.; Ma, J.; Heijnen, C. J.; Dantzer, R.; Scherrer, G.; Kavelaars, A.; Bernard, M.; Aldhamen, Y.; Folger, J. K.; Laumet, G.
Show abstract
Chronic pain often alternates between transient remission and relapse of severe pain. While most research on chronic pain has focused on mechanisms maintaining pain, there is a critical unmet need to understand what prevents pain from re-emerging in those who recover from acute pain. We found that interleukin (IL)-10, a pain resolving cytokine, is persistently produced by resident macrophages in the spinal meninges during remission from pain. IL-10 upregulated expression and analgesic activity of {delta}-opioid receptor ({delta}OR) in the dorsal root ganglion. Genetic or pharmacological inhibition of IL-10 signaling or {delta}OR triggered relapse to pain in both sexes. These data challenge the widespread assumption that remission of pain is simply a return to the naive state before pain was induced. Instead, our findings strongly suggest a novel concept that: remission is a state of lasting pain vulnerability that results from a long-lasting neuroimmune interactions in the nociceptive system.
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