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由IL-1β诱导的中性细胞外细胞陷促进内皮功能障碍,并加剧四肢缺血症

Shigang Lin¹, Pengwei Zhu², Liujun Jiang²

¹Department of Vascular Surgery, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.

Hypertension research : official journal of the Japanese Society of Hypertension

|April 11, 2024

概括

中性粒细胞外细胞陷 (NETs) 在下肢缺血中驱动血管炎症和内皮功能障碍. 抑制NET或IL-1β显示了这种疾病的治疗潜力.

科学领域:

免疫学免疫学免疫学
血管生物学血管生物学
分子医学是分子医学.

背景情况:

血管炎症和内皮功能障碍是血管疾病的关键驱动因素.
中性细胞外细胞陷 (NETs) 涉及病理,但它们在下肢缺血中的作用尚不清楚.

研究的目的:

调查NET在血管炎症和下肢缺血症重塑中的功能意义.
阐明NETs影响内皮细胞和炎症通路的机制.

主要方法:

单细胞RNA测序 (scRNA-seq) 和流细胞测量用于分析中性粒细胞和内皮细胞.
免疫光学和西欧斑点测试用于评估NET形成,细胞因子表达和信号通路 (pSTAT1/STAT1).
在体内研究使用缺血性小鼠模型与NETosis或IL-1β抑制.

主要成果:

在人类四肢缺血症中观察到中性粒细胞的激活和NET形成的增加.
NETs诱导了内皮细胞激活,增加了粘附分子 (VCAM-1,ICAM-1) 和炎症细胞因子 (IL-1β,IL-6),同时降低了VE-cadherin.
通过pSTAT1/STAT1信号通路,NETs调节了内皮功能.
抑制NETosis或IL-1β改善了小鼠的血管炎症和缺血症.

结论:

由IL-1β诱导的NETs通过激活STAT1信号来促进下肢缺血中的内皮激活和炎症.
针对NETs为炎症性血管疾病提供了潜在的治疗策略,包括与四肢缺血相关的疾病.

关键词:

一个IL-1ββ.网络网络网络网络细胞内皮细胞的内皮细胞.这是一种炎症炎症炎症炎症.缺血缺血症是什么意思缺血缺血症

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