暴露于UFP和ACE/ACE2路径之间的相关性:寻找可能参与COVID-19流行病的可能性
Laura Botto1, Alessandra Bulbarelli1,2, Elena Lonati1
1School of Medicine and Surgery, University of Milano-Bicocca, 20900 Monza, Italy.
来自空气污染的超细颗粒 (UFP) 暴露会改变关键蛋白质,增加COVID-19的严重程度. 这强调了空气污染是严重的SARS-CoV-2感染的重要危险因素.
科学领域:
- 环境健康 环境健康
- 肺部病理学 肺部病理学
- 病毒学 病毒学
背景情况:
- 空气污染,特别是大气颗粒物 (PM),与COVID-19爆发严重程度相关.
- 氨酸- ангиотензин系统 (RAS),涉及ACE/AngII/AT1和ACE2/Ang(1-7) /MAS轴,在污染引起的炎症中发挥作用.
- ACE2作为SARS-CoV-2的入口受体,而PM暴露可以增加ACE2的表达.
研究的目的:
- 研究急性和亚急性暴露于超细颗粒 (UFP) 对小鼠ACE2,ACE,COX-2,HO-1和iNOS水平的影响.
- 分析暴露于柴油废气颗粒 (DEP) 和生物质燃烧 (BB) 后这些蛋白质的器官特异性变化.
- 探索UFP诱导的分子变化与严重COVID-19的病原体之间的联系.
主要方法:
- 在暴露研究中使用了体内BALB/c雄性小鼠模型.
- 通过DEP和BB对UFP的急性和亚急性暴露.
- 肺部和其他相关器官中的ACE2,ACE,COX-2,HO-1和iNOS的量化水平.
主要成果:
- 在所有检查的器官中,UFP暴露改变了ACE2和/或ACE水平.
- 亚急性DEP暴露导致可溶性ACE2 (s-ACE2) 的释放.
- 观察到COX-2,HO-1和iNOS的器官特异性变化,表明在UFP诱导的炎症和氧化应激中的作用.
结论:
- 暴露于UFP会破坏参与炎症和氧化应激的蛋白质的调节,可能会加剧COVID-19的严重程度.
- UFP和SARS-CoV-2之间共享的分子通路表明,空气污染增加了对严重COVID-19的脆弱性.
- 空气污染暴露可能导致高污染地区的COVID-19死亡率更高,支持风险分层方法.
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