截断的氧化脂会加剧由细菌病原体引起的内皮功能障碍和肺损伤
Pratap Karki1, Chen-Ou Zhang1, Kamoltip Promnares2
1Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, United States of America.
Cellular signalling
|July 12, 2023
概括
高水平的截断氧化脂 (Tr-OxPLs) 会恶化由细菌感染引起的肺损伤和内皮功能障碍. 这些发现突出了Tr-OxPLs作为败血症和创伤相关的肺损伤的关键风险因素.
科学领域:
- 生物医学科学 生物医学科学
- 免疫学 免疫学 免疫学
- 肺部医学 肺部医学
背景情况:
- 氧化脂 (OxPLs) 在感染,败血症和创伤期间增加.
- 截断的氧化脂 (Tr-OxPLs) 对肺内皮有负面影响.
- 在细菌病原体引起的肺损伤中Tr-OxPLs的作用尚未完全理解.
研究的目的:
- 调查六种Tr-OxPL物种对内皮通透性和炎症反应的影响.
- 在小鼠模型中确定Tr-OxPLs对细菌颗粒诱导的肺损伤的影响.
主要方法:
- 经过测试的Tr-OxPLs (KOdiA-PC,POV-PC,PON-PC,PAz-PC,PGPC,Lyso-PC) 用于使用VE-cadherin免疫和超内皮电阻对内皮屏障功能的影响.
- 评估的炎症反应包括NF-κB激活,IL-6/IL-8分泌和ICAM-1/VCAM-1表达.
- 使用一种由热杀死金黄色葡萄球菌 (HKSA) 诱导的急性肺损伤的小鼠模型与静脉注射Tr-OxPLs,通过Evans Blue测量BAL蛋白,细胞计数,细胞因子表达和血管泄漏.
主要成果:
- 所有测试的Tr-OxPL都加剧了由HKSA引起的内皮屏障破坏.
- Tr-OxPLs增强了HKSA诱导的NF-κB激活,IL-6/IL-8分泌,以及ICAM-1/VCAM-1表达.
- 在体内,Tr-OxPLs恶化了HKSA诱导的肺损伤,增加了BAL蛋白和细胞计数,促进了炎症 (TNFα,KC,IL1β,CCL2),并增强了血管泄漏.
结论:
- 升高的Tr-OxPL显著恶化细菌病原体诱导的内皮功能障碍和急性肺损伤.
- 在细菌感染期间,Tr-OxPLs在肺损伤的发病过程中起到关键风险因素的作用.
- 这些发现强调了Tr-OxPLs在炎症反应中的重要性,并表明了潜在的治疗点.
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