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
胶质瘢痕
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,Mark J. Zylka
出处
期刊:Neuron
[Cell Press]
日期:2021-03-05
卷期号:109 (8): 1274-1282.e6
被引量:119
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.
科研通智能强力驱动
Strongly Powered by AbleSci AI