趋化因子介导的神经炎症反应和神经病理性疼痛

各种疾病引起的神经系统的损伤或功能障碍致使全球数以百万计的人们患有神经性病理性疼痛。目前的方法对神经病理性疼痛的疗效不佳且有副作用，需要开发有效的治疗方法。近年来人们逐渐认识到，脊髓中胶质细胞（如小胶质细胞和星形胶质细胞）能通过释放强效的神经调质，如促炎细胞因子和趋化因子，在神经性病理性疼痛的产生和维持中起重要作用。近期的证据显示，趋化因子是疼痛调控中的新成员。该文综述了一些趋化因子和受体（如CCL2／CCR2、CXCL1／CXCR2、CX3CL1／CX3CR1、CCL21／CXCR3）作为神经元和胶质细胞相互调控的介质参与神经病理性疼痛的调节。靶向趋化因子介导的神经炎症反应将成为治疗神经病理性疼痛的新方向。

Chemokine-Mediated Neuroinflammation and Neuropathic Pain

Millions of people worldwide suffer from neuropathic pain as a result of damage to or dysfunc- tion 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 proin- flammatory 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 modu- lating neuropathic pain. Targeting chemokine-mediated neuroinflammation will be a new approach for treatment of neuropathic pain.