Neuroimmune Interactions and Pain

Chronic pain imposes a tremendous burden on the sufferer’s quality of life. Mounting evidence supports a critical role for neuroimmune interactions in the development and maintenance of chronic pain. Nerve injury leads to the activation of glia via sphingosine-1-phosphate, Toll-like receptors, chemokines, neuropeptides, and purinergic receptors. In turn, activated glia influence neuronal activity via interleukin 1β, tumor necrosis factor, brain-derived neurotrophic factor, reactive oxygen species, and excitatory amino acids. Epigenetic mechanisms of neuroimmune communication are also discussed. Investigation of neuroimmune interactions after peripheral nerve injury broadens our understanding of the mechanisms that drive neuropathic pain, and such interactions provide potential therapeutic targets for managing neuropathic pain.