暴露于颗粒物会通过抑制表皮的抗病毒反应来增强SARS-CoV-2三角洲变种感染的潜力
Supasek Kongsomros1,2, Jiraporn Paha3, Phayungsap Prasara-A3
1Chakri Naruebodindra Medical Institute, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Samutprakarn, Thailand.
Frontiers in cellular and infection microbiology
|January 21, 2026
概括
粗颗粒物 (PM10) 通过削弱细胞防御来恶化德尔塔变种COVID-19感染. 这种空气污染暴露会损害亡并减少关键的细胞因子反应,使细胞更容易受到病毒复制的影响.
科学领域:
- 环境健康 环境健康
- 病毒学 病毒学
- 细胞生物学 细胞生物学
背景情况:
- 空气中的颗粒物 (PM),特别是PM2.5和PM10,是环境健康的重大风险.
- 流行病学研究表明,PM暴露可能会加剧COVID-19的结果,但细胞机制尚不清楚.
研究的目的:
- 研究PM2.5和PM10预暴露对人类上皮细胞中SARS-CoV-2感染动态的影响.
- 阐明PM影响病毒病原性的细胞机制.
主要方法:
- 卡卢-3人类上皮细胞被预先暴露在PM2.5或PM10.0中.
- 随后,细胞被野生型的SARS-CoV-2或Delta变种感染.
- 分析了病毒感染,受体表达,细胞亡和细胞因子反应.
主要成果:
- PM10,而不是PM2.5,显著增强了Delta变种感染,增加了受感染的细胞和病毒标位.
- 这种增强与抗病毒防御功能受损有关,包括抑制亡和减少促炎性细胞因子表达 (IFN-γ,IP-10,TNF-α).
- ACE2受体表达和病毒进入效率不受PM暴露前影响.
结论:
- PM10通过抑制细胞灭亡和炎症信号传递,损害了表皮的抗病毒反应.
- 这使得细胞环境对SARS-CoV-2复制更加宽容,特别是对Delta变种更宽容.
- 这些发现提供了空气污染和COVID-19严重程度增加之间的机制联系,突出了公共卫生影响.
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