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中性粒细胞外细胞陷在创伤性脑损伤期间加剧中性粒细胞反向超内皮细胞迁移

Ruitian Zhou¹, Tong Zhang², Jianbin Sun²

¹Department of Biochemistry and Molecular Biology, School of Basic Medicine, Army Medical University, Chongqing, 400038, China; Battalion 5, Brigade 2 of Medical Undergraduate, School of Basic Medicine, Army Medical University, Chongqing, 400038, China.

Biochemical and biophysical research communications

|July 29, 2025

概括

在创伤性脑损伤 (TBI) 中,中性粒细胞的反向跨内皮移动 (rTEM) 被中性粒细胞外细胞陷 (NET) 促进. 抑制NETs可以减少RTEM,帮助创伤后的神经恢复.

科学领域:

免疫学免疫学免疫学
神经科学是一个神经科学.
细胞生物学细胞生物学

背景情况:

中性粒细胞从血管迁移到组织中,以对抗感染.
反向跨内皮移动 (rTEM) 允许中性粒细胞重返循环,可能扩散炎症.
对于rTEM的机制,特别是在机械损伤后,如创伤性脑损伤 (TBI),尚不清楚.

研究的目的:

在小鼠TBI模型中研究调节中性粒细胞rTEM的机制.
在TBI后确定促进中性粒细胞rTEM的因素.
评估针对RTEM治疗TBI恢复的治疗潜力.

主要方法:

建立了TBI的小鼠机械伤害模型.
在体内使用LY6G-生物素/斯特雷普塔维丁 (STREPT) 交联用于中性粒细胞标签.
在体外仿真中采用内皮/中性粒细胞双转孔试剂.
评估ICAM-1和JAM-C.的表达.
在体内使用NETs抑制剂Cl-Amidine.

主要成果:

在TBI急性阶段观察到中性粒细胞rTEM,中性粒细胞迁移到骨髓.
在迁移性中性粒细胞上发现高ICAM-1表达,与大脑组织中的NETs水平相关.
证明NETs可以减少内皮JAM-C,并在体外增加中性粒细胞ICAM-1表达.
Cl-Amidine治疗减少了中性粒细胞的rTEM,并在TBI后改善了神经恢复和炎症解决.

结论:

在TBI中,NETs通过降解内皮JAM-C和调高中性粒细胞ICAM-1来促进中性粒细胞rTEM.
在TBI后,rTEM有助于中性粒细胞在外周器官的分布.
针对NETs介导的RTEM是TBI的一个有前途的治疗策略.

关键词:

在 ICAM-1 中,这就是JAM-C.网络网络网络网络中性粒细胞的逆迁移.这是一个TBI,TBI.

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