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对DEP和PM的亚毒性暴露_2.5 通过细胞内颗粒积累损害了树突细胞功能

Yuki Nakahira¹, Daisuke Otomo¹, Tomoaki Okuda²

¹Department of Pharmaceutical Sciences, Kobe Gakuin University, Kobe 650-8586, Japan.

Journal of xenobiotics

|September 22, 2025

概括

细颗粒物 (PM2.5) 和柴油废气颗粒 (DEP) 造成的空气污染会损害免疫细胞,但不会导致细胞死亡. 这种非细胞毒性作用会损害抗病毒防御,增加感染风险.

科学领域:

免疫学免疫学免疫学
环境健康环境健康
毒理学毒理学毒理学

背景情况:

空气污染,特别是细颗粒物 (PM2.5) 和柴油废气颗粒 (DEP),是严重的健康风险.
DEP含有与炎症,氧化应激和免疫功能障碍相关的反应性成分.
对于PM2.5和DEP对细胞功能的亚毒性影响尚不清楚.

研究的目的:

研究低毒性PM2.5和DEP对树突细胞 (DC) 功能的影响.
探索非细胞毒性颗粒物引起的免疫损伤背后的机制.

主要方法:

在暴露研究中使用了人体血细胞系DC样细胞系PMDC05.
在非细胞毒性度下暴露于PM2.5和DEP的细胞.
评估细胞功能,包括在托尔类受体 (TLR) 刺激后的颗粒吸收,内细胞化,细胞化和基因表达.

主要成果:

PM2.5和DEPs在DC中以最小的细胞毒性在细胞内积累.
在TLR7刺激后观察到受损的内细胞,细胞和干扰素基因表达.
功能缺陷是特异性的TLR7刺激,而不是TLR4,表明选择性内分泌体通路破坏.
这些损伤发生在没有可测量的细胞死亡 (LDH释放) 的情况下.

结论:

在非细胞毒性水平上,PM2.5和DEP可以损害先天免疫反应和树突细胞功能.
Lysosomal 过载和改变的细胞内流通可能是损伤的机制.
空气中的颗粒物污染可能通过非细胞毒性途径损害抗病毒免疫力,增加感染易感性.
维护 lysosomal 完整性的策略可以减轻空气污染的免疫毒性影响.

关键词:

对于PM2.5来说,这是一个很好的例子.在TLR7信号系统中.树突细胞是一种树突细胞.柴油废气颗粒的使用情况溶酶体功能障碍溶酶体功能障碍

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