病毒感染后表面发起的非血栓生成血块形成的分子基础
Kao Li1,2, Kuan-Che Feng2, Marcia Simon3
1School of Biomedicine and Nursing, Shandong Institute of Petroleum and Chemical Technology, Dongying 257061, Shandong, China.
ACS applied materials & interfaces
|June 7, 2024
概括
病毒感染引发炎症反应,包括纤维素素升高和脂质释放,导致非血栓凝块的形成. 这项研究揭示了受感染细胞的脂质在表面上启动了这种自发纤维形成.
科学领域:
- 生物化学 生物化学
- 免疫学 免疫学 免疫学
- 病理学 病理学 病理学
背景情况:
- 病毒感染引起炎症反应,包括纤维素素水平的增加和脂质滴积累.
- 非血介导的血块形成是一个公认的现象,但其与病毒感染启动的联系尚未完全理解.
研究的目的:
- 研究将病毒感染诱导的炎症与非血栓生成的血块形成的启动联系在一起的分子机制.
- 为了确定病毒暴露后自发纤维化发生的特定因素.
主要方法:
- 人类上皮细胞和马丁-达比犬 (MDCK) 细胞被H1N1,OC43和腺病毒感染.
- 来自受感染细胞的条件介质被用于治疗人类静脉内皮细胞和人类肺部微血管内皮细胞.
- 纤维生成在暴露于纤维素的细胞表面上进行了评估,有或没有直接的病毒或条件介质暴露. 采用了接触角度测和免疫组织化学.
主要成果:
- 暴露于受感染细胞条件介质的上皮细胞和内皮细胞在没有血栓的纤维素涂层表面上启动了纤维生成.
- 直接病毒暴露或SARS-CoV-2尖端蛋白暴露没有诱导纤维形成.
- 条件介质中的脂质,可能来自死去的感染细胞,形成了疏水性残留物,启动了纤维生成,这个过程不受加热到60°C的影响.
结论:
- 病毒感染诱导的炎症反应,特别是脂质释放,创造了有利于表面启动的,非血栓凝块形成的条件.
- 这项研究阐明了一种新的途径,即病毒感染期间细胞脂质的积累和释放直接促进自发血块形成.
- 这些发现表明,对病毒病原体的常见炎症反应与血栓事件的可能性之间存在联系.
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