柴油废气颗粒诱导极化状态依赖于人类单细胞衍生的巨细胞的功能和转录变化
Timothy Smyth1,2, Ilona Jaspers1,2,3
1Curriculum in Toxicology & Environmental Medicine, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States.
American journal of physiology. Lung cellular and molecular physiology
|December 12, 2023
概括
柴油废气颗粒 (DEP) 暴露会产生混合的M1/M2炎症性巨细胞表型,特别影响M1巨细胞. 这种颗粒物 (PM) 暴露可能会使呼吸道感染的结果恶化.
科学领域:
- 免疫学和呼吸系统医学
- 环境健康科学 环境健康科学
背景情况:
- 巨细胞存在于从促炎 (M1) 到促溶解 (M2) 状态的频谱中,并且可以在两者之间重新编程.
- 颗粒物 (PM),包括柴油废气颗粒 (DEP),与不良的呼吸系统健康结果有关,并改变巨细胞的功能.
研究的目的:
- 研究DEP对人类单细胞衍生巨细胞 (hMDMs) 的偏振依赖作用.
- 为了确定DEP暴露是否会在M1和M2状态之间改变巨细胞重编程.
主要方法:
- 隔离人类单细胞并使用M-CSF将其分化为巨细胞.
- 极化巨细胞到M2状态或未极化,然后暴露于DEP,M1刺激 (IFN-γ和LPS),或两者兼而有之.
- 评估了细胞功能,分泌特征,基因表达和生物能量学.
主要成果:
- 与之前的报道相反,DEP暴露导致重新编程的M2巨细胞中混合的M1/M2表型.
- 在所有巨细胞极化状态中,DEP暴露损害了细胞功能.
- 在M1巨细胞中,DEP优先改变了生物能量特性.
结论:
- 重编程的M2巨细胞的DEP暴露产生了一个高度炎症的,有活力的亚群.
- M1巨细胞对DEP特别敏感,表现出减少的细胞分裂和改变的生物能量.
- 这些DEP诱导的巨细胞变化可能导致在呼吸道感染期间暴露于PM后的健康状况不佳.
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