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中性粒细胞胞外诱捕网加剧继发性损伤，促进脊髓损伤后的神经炎症和血脊髓屏障破坏。

Neutrophil Extracellular Traps Exacerbate Secondary Injury Promoting Neuroinflammation and Blood-Spinal Cord Barrier Disruption in Spinal Cord Injury.

机构信息

Department of Rehabilitation, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.

Department of Neurosurgery, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.

出版信息

Front Immunol. 2021 Aug 11;12:698249. doi: 10.3389/fimmu.2021.698249. eCollection 2021.

DOI:10.3389/fimmu.2021.698249
PMID:34456910
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8385494/
Abstract

As the first inflammatory cell recruited to the site of spinal cord injury (SCI), neutrophils were reported to be detrimental to SCI. However, the precise mechanisms as to how neutrophils exacerbate SCI remain largely obscure. In the present study, we demonstrated that infiltrated neutrophils produce neutrophil extracellular traps (NETs), which subsequently promote neuroinflammation and blood-spinal cord barrier disruption to aggravate spinal cord edema and neuronal apoptosis following SCI in rats. Both inhibition of NETs formation by peptidylarginine deiminase 4 (PAD4) inhibitor and disruption of NETs by DNase 1 alleviate secondary damage, thus restraining scar formation and promoting functional recovery after SCI. Furthermore, we found that NETs exacerbate SCI partly elevating transient receptor potential vanilloid type 4 (TRPV4) level in the injured spinal cord. Therefore, our results indicate that NETs might be a promising therapeutic target for SCI.

摘要

作为第一个被招募到脊髓损伤（SCI）部位的炎症细胞，中性粒细胞被报道对 SCI 有害。然而，中性粒细胞加剧 SCI 的精确机制在很大程度上仍不清楚。在本研究中，我们表明浸润的中性粒细胞产生中性粒细胞胞外诱捕网（NETs），随后促进神经炎症和血脊髓屏障破坏，加重大鼠 SCI 后的脊髓水肿和神经元凋亡。PAD4 抑制剂抑制 NETs 形成和 DNase 1 破坏 NETs 均可减轻继发性损伤，从而抑制 SCI 后的瘢痕形成和促进功能恢复。此外，我们发现 NETs 通过升高损伤脊髓中瞬时受体电位香草酸亚型 4（TRPV4）水平部分加剧 SCI。因此，我们的结果表明 NETs 可能是 SCI 的一个有前途的治疗靶点。

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