Microglia and monocytes synergistically promote the transition from acute to chronic pain after nerve injury.

Microglia and monocytes synergistically promote the transition from acute to chronic pain after nerve injury.
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小胶质细胞和单核细胞协同促进神经损伤后从急性到慢性疼痛的过渡。

DOI:
10.1038/ncomms12029
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发表时间:
2016-06-28
影响因子:
16.6
通讯作者:
Wu LJ
Wu LJ
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Peng J;Gu N;Zhou L;B Eyo U;Murugan M;Gan WB;Wu LJ

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小胶质细胞和外周血单核细胞在神经病理性疼痛的啮齿动物模型中起到了超敏作用。然而,在这些模型中,小胶质细胞和外周血单核细胞各自的确切功能还没有被研究。为了解决这个问题,我们结合转基因小鼠和药理学工具,在脊髓神经横断术(SNT)的小鼠模型中,特异性和时间性地控制小胶质细胞和单核细胞的耗竭。我们发现,虽然小胶质细胞和单核细胞在机械痛觉过敏或热痛觉过敏的启动过程中是必需的,但这些细胞对维持超敏反应可能不那么重要。此外,我们证明,无论是常驻的小胶质细胞还是外周单核细胞,都足以控制SNT后的神经病理性疼痛。我们认为,周围神经损伤后,驻留的小胶质细胞和外周单核细胞协同作用,启动超敏反应,促进从急性疼痛向慢性疼痛的转变。小胶质细胞和单核细胞参与了神经病理性疼痛状态,但这两种细胞类型的确切作用尚不清楚。在这里,彭等人。在小鼠中使用时间可控的单核细胞和小胶质细胞消融,以表明这些细胞共同作用,启动神经病理性疼痛样行为,但在维持阶段不那么重要。
Microglia and peripheral monocytes contribute to hypersensitivity in rodent models of neuropathic pain. However, the precise respective function of microglia and peripheral monocytes has not been investigated in these models. To address this question, here we combined transgenic mice and pharmacological tools to specifically and temporally control the depletion of microglia and monocytes in a mouse model of spinal nerve transection (SNT). We found that although microglia and monocytes are required during the initiation of mechanical allodynia or thermal hyperalgesia, these cells may not be as important for the maintenance of hypersensitivity. Moreover, we demonstrated that either resident microglia or peripheral monocytes are sufficient in gating neuropathic pain after SNT. We propose that resident microglia and peripheral monocytes act synergistically to initiate hypersensitivity and promote the transition from acute to chronic pain after peripheral nerve injury. Microglia and monocytes contribute to neuropathic pain states, but the precise role of the two cell types is not clear. Here Peng et al. use temporally controlled ablation of monocytes and microglia in mice to show that these cells work together to initiate neuropathic-pain like behaviour, but are less important in the maintenance phase.