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地铁细颗粒 (PM_2.5) 诱导的促炎反应触发了通过TLRs/NF-κB依赖途径的气道上皮质屏障损伤

Fanmei Zeng¹, Guanhua Pang¹, Liwen Hu²

¹Department of Environmental Health, School of Public Health, China Medical University, Shenyang, China.

Environmental toxicology

|August 27, 2024

概括

地铁细颗粒物 (PM2.5) 触发呼吸道炎症并通过影响细胞因子释放和紧密的结合,损害细胞. 这一途径涉及收费类受体 (TLR) 和核因子-kappa B (NF-κB).

科学领域:

环境健康环境健康
毒理学毒理学毒理学
细胞生物学细胞生物学

背景情况:

地铁细颗粒物 (PM2.5) 是城市人口的主要暴露来源.
暴露于PM2.5与急性炎症损伤有关,但确切的机制尚不清楚.
了解地铁PM2.5对呼吸道上皮细胞的影响对于公共卫生至关重要.

研究的目的:

阐明地铁PM2.5在人类支气管上皮细胞 (BEAS-2B) 中引起气道损伤的机制.
为了研究促炎性细胞因子和紧结蛋白的作用.
为了确定PM2.5引起的气道损伤所涉及的信号通路.

主要方法:

暴露BEAS-2B细胞在地下PM2.5.5的不同度下.
测量促炎性细胞因子 (IL-17E,TNF-α,TGF-β,TSLP) 和紧结蛋白 (ZO-1,E-cadherin,occludin) 的表达.
评估TLRs/NF-κB通路抑制剂,酸盐树脂和德胺对PM2.5诱导的变化的影响.

主要成果:

地下PM2.5剂量依赖于BEAS-2B细胞的炎症促细胞因子释放的增加.
暴露在PM2.5下降了紧密结蛋白的表达 (zonula occludens-1,E-cadherin,occludin) 在剂量依赖的方式.
收费类受体 (TLRs) 和核因子-kappa B (NF-κB) 的抑制剂,以及特定的化剂,改善了PM2.5诱导的细胞因子和紧结变化.

结论:

地铁PM2.5诱导呼吸道上皮损伤,最初增加细胞因子表达,随后降低紧密结合的完整性.
观察到的效应是通过激活TLRs/NF-κB信号通路来实现的.
地铁PM2.5内的金属组件可能在引起气道上皮损伤方面发挥重要作用.

关键词:

呼吸道上皮质呼吸道上皮质炎症性伤害的伤害.地铁中的PM2.5 紧密的交叉路口紧密的连接类似于收费的接收器.

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