Recent evidence demonstrates that peripheral immune cells contribute to the nociceptive hypersensitivity associated with neuropathic pain by infiltrating the central nervous system (CNS). We have recently developed a rat model of graded chronic constriction injury (CCI) by varying the exposure of the sciatic nerve and control non-nerve tissue to surgical placement of chromic gut. We demonstrate that splenocytes can contribute significantly to CCI-induced allodynia, as adoptive transfer of these cells from high pain donors to low pain recipients potentiates allodynia (P<0.001). The phenomenon was replicated with peripheral blood mononuclear cells (P<0.001). Adoptive transfer of allodynia was not achieved in sham recipients, indicating that peripheral immune cells are only capable of potentiating existing allodynia, rather than establishing allodynia. As adoptively transferred cells were found by flow cytometry to migrate to the spleen (P<0.05) and potentiation of allodynia was prevented in splenectomised low pain recipients, adoptive transfer of high pain splenocytes may induce the migration of host-derived immune cells from the spleen to the CNS as observed by flow cytometry (P<0.05). Importantly, intrathecal transfer of CD45(+) cells prepared from spinal cords of high pain donors into low pain recipients led to potentiated allodynia (P<0.001), confirming that infiltrating immune cells are not passive bystanders, but actively contribute to nociceptive hypersensitivity in the lumbar spinal cord.

译文

最近的证据表明,外周免疫细胞通过浸润中枢神经系统 (CNS) 而导致与神经性疼痛相关的伤害性超敏反应。我们最近通过改变坐骨神经的暴露并控制非神经组织对肠肠的外科手术放置,开发了分级慢性收缩损伤 (CCI) 的大鼠模型。我们证明,脾细胞可以显着促进CCI诱导的异常性疼痛,因为这些细胞从高疼痛供体到低疼痛受体的过继转移会增强异常性疼痛 (P<0.001)。用外周血单个核细胞复制该现象 (P<0.001)。假接受者未实现异常性疼痛的过继转移,这表明外周免疫细胞仅能够增强现有的异常性疼痛,而不是建立异常性疼痛。由于通过流式细胞术发现过继转移的细胞迁移到脾脏 (P<0.05),并且在脾切除的低疼痛受体中防止了异常性疼痛的增强,通过流式细胞术观察到,高疼痛脾细胞的过继转移可能诱导宿主来源的免疫细胞从脾迁移到CNS (P<0.05)。重要的是,鞘内转移从高疼痛供体的脊髓制备的CD45(+) 细胞到低疼痛受体导致增强的异常性疼痛 (P<0.001),证实浸润的免疫细胞不是被动的旁观者,而是积极地促进腰椎脊髓的伤害性超敏反应。

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