日本九州大学Makoto Tsuda研究组，发现一个参与缓解和复发神经性疼痛的脊髓小胶质细胞群。2022年4月1日，国际知名学术期刊《科学》发表了这一成果。

他们发现表达 CD11c 的脊髓小胶质细胞出现在神经损伤后发生行为疼痛超敏反应之后。 脊髓 CD11c+ 小胶质细胞耗竭的神经损伤小鼠未能从这种超敏反应中自发恢复。CD11c+ 小胶质细胞表达胰岛素样生长因子-1 (IGF1)，并且对 IGF1 信号传导的干扰概括了疼痛恢复的损害。在疼痛恢复的小鼠中，CD11c+ 小胶质细胞的耗竭或 IGF1 信号传导的中断导致疼痛超敏反应的复发。他们的研究结果揭示了神经性疼痛缓解和复发的机制，为治疗策略提供了潜在的目标。

据介绍，神经性疼痛通常由影响躯体感觉系统的损伤和疾病引起。尽管已经对疼痛的发展进行了很好的研究，但疼痛恢复机制仍然很大程度上未知。

附：英文原文

Title: A spinal microglia population involved in remitting and relapsing neuropathic pain

Author: Keita Kohno, Ryoji Shirasaka, Kohei Yoshihara, Satsuki Mikuriya, Kaori Tanaka, Keiko Takanami, Kazuhide Inoue, Hirotaka Sakamoto, Yasuyuki Ohkawa, Takahiro Masuda, Makoto Tsuda

Issue&Volume: 2022-04-01

Abstract: Neuropathic pain is often caused by injury and diseases that affect the somatosensory system. Although pain development has been well studied, pain recovery mechanisms remain largely unknown. Here, we found that CD11c-expressing spinal microglia appear after the development of behavioral pain hypersensitivity following nerve injury. Nerve-injured mice with spinal CD11c+ microglial depletion failed to recover spontaneously from this hypersensitivity. CD11c+ microglia expressed insulin-like growth factor-1 (IGF1), and interference with IGF1 signaling recapitulated the impairment in pain recovery. In pain-recovered mice, the depletion of CD11c+ microglia or the interruption of IGF1 signaling resulted in a relapse in pain hypersensitivity. Our findings reveal a mechanism for the remission and recurrence of neuropathic pain, providing potential targets for therapeutic strategies.

DOI: abf6805

Source: https://www.science.org/doi/10.1126/science.abf6805