星形胶质增生
医学
周围神经损伤
脊髓
神经病理性疼痛
神经炎症
炎症
伤害
脊髓损伤
伤害感受器
病理
神经科学
神经损伤
免疫学
麻醉
中枢神经系统
生物
受体
坐骨神经
内科学
精神科
作者
Jesse K. Niehaus,Bonnie Taylor-Blake,Lipin Loo,Jeremy M. Simon
出处
期刊:Neuron
[Elsevier]
日期:2021-04-01
卷期号:109 (8): 1274-1282.e6
被引量:58
标识
DOI:10.1016/j.neuron.2021.02.018
摘要
Peripheral nerve injury induces long-term pro-inflammatory responses in spinal cord glial cells that facilitate neuropathic pain, but the identity of endogenous cells that resolve spinal inflammation has not been determined. Guided by single-cell RNA sequencing (scRNA-seq), we found that MRC1+ spinal cord macrophages proliferated and upregulated the anti-inflammatory mediator Cd163 in mice following superficial injury (SI; nerve intact), but this response was blunted in nerve-injured animals. Depleting spinal macrophages in SI animals promoted microgliosis and caused mechanical hypersensitivity to persist. Conversely, expressing Cd163 in spinal macrophages increased Interleukin 10 expression, attenuated micro- and astrogliosis, and enduringly alleviated mechanical and thermal hypersensitivity in nerve-injured animals. Our data indicate that MRC1+ spinal macrophages actively restrain glia to limit neuroinflammation and resolve mechanical pain following a superficial injury. Moreover, we show that spinal macrophages from nerve-injured animals mount a dampened anti-inflammatory response but can be therapeutically coaxed to promote long-lasting recovery of neuropathic pain.
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