perfluoroalkyl物质 (PFAS) 影响肺细胞和组织的炎症
Julie Dragon1, Michael Hoaglund1, Appala Raju Badireddy1
1Department of Pathology and Laboratory Medicine, Larner College of Medicine, University of Vermont, Burlington, VT 05405, USA.
International journal of molecular sciences
|May 27, 2023
概括
暴露于和多醇基物质 (PFAS) 可以通过激活炎症体和改变细胞膜来损害肺部. 这项研究将PFAS与肺炎和潜在的喘发展联系在一起.
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:
- 与和多基物质 (PFAS) 相关的不良肺结局已被认可,但潜在的机制尚不清楚.
- 了解PFAS如何影响肺细胞和炎症途径对于评估健康风险至关重要.
研究的目的:
- 研究短链和长链PFAS影响人类支气管上皮细胞的细胞机制.
- 为了检查NLRP3炎症酶的激活和PFAS暴露后细胞膜性质的改变.
- 分析 perfluorooctanoic 酸 (PFOA) 对具有不同 PPARα 活性的小鼠肺部基因表达的影响.
主要方法:
- 人类支气管上皮细胞暴露于各种度的短链 (如GenX) 和长链 (如PFOA,PFOS) PFAS,以确定细胞毒性水平.
- 使用非细胞毒性PFAS度来评估NLRP3炎症酶原始化和激活.
- 原子力显微镜评估了细胞膜性质的变化.
- 在长期暴露于PFOA后,RNA测序分析了小鼠肺中的基因表达.
主要成果:
- 酸和 perfluorooctane sulfonic acid (PFOS) 启动并激活了肺细胞中的NLRP3炎症体.
- PFOA显著改变了细胞膜的特性,而PFOS没有.
- 在小鼠中,PFOA暴露导致了炎症和免疫相关基因的显著变化,特别是在野生类型和PPARα变体中.
结论:
- 暴露于PFAS可以显著改变肺部生物学,包括炎症酶激活和基因表达.
- 观察到的变化表明PFAS在喘和气道过敏反应的发展中可能发挥作用.
- 进一步研究PFAS毒理学和肺损伤机制是有必要的.
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