• Qin Yin, Qin Fan, Yu Zhao, Ming-Yue Cheng, He Liu, Jing Li, Fei-Fei Lu, Jin-Tai Jia, Wei Cheng, and Chang-Dong Yan.
• Xuzhou Medical College, Xuzhou, China; Jiangsu Province Key Laboratory of Anesthesiology and Center for Pain Research and Treatment; Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou, China; Affiliated Hospital of Xuzhou Medical College, Xuzhou, China.
• Plos One. 2015 Jan 1;10(1):e0115120.

BackgroundThe NF-κB pathway and chemokine (C-C motif) ligand 5 (CCL5) are involved in pain modulation; however, the precise mechanisms of their interactions in chronic neuropathic pain have yet to be established.MethodsThe present study examined the roles of spinal NF-κB and CCL5 in a neuropathic pain model after chronic constriction injury (CCI) surgery. CCI-induced pain facilitation was evaluated using the Plantar and von Frey tests. The changes in NF-κB and CCL5 expression were analyzed by immunohistochemistry and Western blot analyses.ResultsSpinal NF-κB and CCL5 expression increased after CCI surgery. Repeated intrathecal infusions of pyrrolidine dithiocarbamate (PDTC, a NF-κB inhibitor) decreased CCL5 expression, inhibited the activation of microglia and astrocytes, and attenuated CCI-induced allodynia and hyperalgesia. Intrathecal injection of a CCL5-neutralizing antibody attenuated CCI-induced pain facilitation and also suppressed spinal glial cell activation after CCI surgery. However, the CCL5-neutralizing antibody did not affect NF-κB expression. Furthermore, selective glial inhibitors, minocycline and fluorocitrate, attenuated the hyperalgesia induced by intrathecal CCL5.ConclusionsThe inhibition of spinal CCL5 expression may provide a new method to prevent and treat nerve injury-induced neuropathic pain.

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