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Chemokine-Mediated Neuroinflammation and Neuropathic Pain
Gao Yongjing*, Zhang Zhijun, Cao Deli
Pain Research Laboratory, Institute of Nautical Medicine, Nantong University, Nantong 226001, China
Abstract: Millions of people worldwide suffer from neuropathic pain as a result of damage to or dysfunction of the nervous system under various disease conditions. Treatment of neuropathic pain is always accompanied by a poor response and undesired adverse effects. Development of effective therapeutic strategy is critical in this field. It has been increasingly recognized that spinal cord glial cells (such as microglia and astrocytes) play a critical role in the induction and maintenance of neuropathic pain by releasing powerful neuromodulators such as proinflammatory cytokines and chemokines. Recent evidence revealed chemokines as new players in pain control. In this paper, we demonstrated that different chemokines and chemokine receptors (e.g., CCL2/CCR2, CXCL1/CXCR2, CX3CL1/CX3CR1, and CCL21/CXCR3) serve as mediators for neuron–glia communication subsequently modulating neuropathic pain. Targeting chemokine-mediated neuroinflammation will be a new approach for treatment of neuropathic pain.