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柴油废气颗粒暴露会加剧状和上皮屏障功能障碍在多状支气管上皮的模型中

Eunsook Park¹, Bu-Yeo Kim², Seahyoung Lee³

¹Division of Allergy and Respiratory Disease Research, Department of Chronic Disease Convergence Research, Korea National Institute of Health, Korea Disease Control and Prevention Agency, Chungju, Chungcheongbuk-do 28159, South Korea.

Ecotoxicology and environmental safety

|February 16, 2024

概括

柴油废气颗粒 (DEP) 是颗粒物2.5 (PM2.5) 的组成部分,会损害气道上皮防御. 暴露于PM2.5会损害乳毛,并破坏上皮屏障,增加肺损伤介质.

科学领域:

呼吸系统生物学呼吸系统生物学
环境毒理学环境毒理学
细胞和分子生物学是细胞和分子生物学.

背景情况:

呼吸道上皮是对吸入刺激物的关键防御障碍.
颗粒物2.5 (PM2.5) 加剧呼吸道疾病,但其对气道粘膜清除的直接影响尚未完全理解.
柴油废气颗粒 (DEP) 是PM2.5.5的主要组成部分.

研究的目的:

用体外气道模型研究DEP对粘膜干净的影响.
分析DEP暴露引起的基因表达变化和细胞变化.
评估DEP诱导的粘膜膜功能障碍对炎症和纤维化介质释放的影响.

主要方法:

使用了两个3D体外气道模型:EpiAirway全厚度 (FT) 和基于正常人类支气管上皮细胞 (NHBE) 的空气-液体接口 (ALI).
暴露于DEP的模型并进行RNA测序 (RNA-Seq) 分析.
量化状细胞数量,状细胞长度,基因表达 (状细胞相关的,MUC5AC,上皮结蛋白) 和介质释放.

主要成果:

暴露于DEP减少了纤毛细胞数量和纤毛长度.
纤毛相关基因的表达减少,而MUC5AC的表达增加.
表皮连接蛋白 (ZO1,Occludin,E-cadherin) 的下调,表明屏障破坏.
暴露于DEP导致炎症和纤维化介质 (IL-1β,IL-6,IL-8,GM-CSF,MMP-1,VEGF,S100A9) 的释放增加.

结论:

DEP会导致气道上皮的状功能障碍和杯状细胞增生.
暴露于DEP会破坏上皮屏障的完整性.
粘膜细胞清除和屏障功能受损促进肺损伤媒介的释放,这表明PM2.5会加剧肺损伤.

关键词:

空气 - 液体接口接口纤维细胞功能纤维细胞功能柴油汽车的废气颗粒是什么?粘膜细胞的清除.正常的人类支气管上皮细胞正常.

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