由可呼吸的微型和纳米聚乙烯颗粒引起的无菌炎症在肺部疾病的发病过程中起作用
Laganà Antonio1,2, Giuseppa Visalli1, Alessio Facciolà1
1Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, Via Consolare Valeria, 98125 Messina, Italy.
Toxicology research
|September 5, 2024
概括
空气中的微塑料和纳米塑料会导致肺细胞的无菌炎症. 氧化塑料加剧了这些影响,激活了NF-kB和NLRP3炎症酶等炎症途径.
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:
- 可呼吸的微型和纳米塑料在环境和室内空气中越来越普遍.
- 这些颗粒有助于无菌炎症,这是肺部疾病发病的关键因素.
- 与空气中的塑料颗粒暴露相关的人类健康风险越来越令人担忧.
研究的目的:
- 研究原始和氧化聚乙烯纳米塑料 (nPS) 和微塑料 (mPS) 对人类肺细胞 (A549) 和单细胞 (THP-1) 的促炎作用.
- 检查A549细胞在通过可溶性因子向单细胞传递炎症信号中的作用.
- 为了阐明塑料颗粒暴露激活的特定炎症途径.
主要方法:
- A549和THP-1细胞系暴露于处女 (v-) 和氧化 (ox-) nPS和mPS (0.1和1微米).
- 使用动态光散射 (DLS) 和蛋白质测量分析蛋白质冠状.
- 通过实时PCR和ELISA测定评估细胞反应,包括Bax/Bcl-2比率,p65 (NF-kB) 表达和IL-1β水平.
主要成果:
- 处女和氧化nPS/mPS都诱导了促炎作用,由A549细胞中改变的Bax/Bcl-2比率证明,抑制了亡.
- 暴露于ox-nPS和v-/ox-mPS导致p65过度表达,证实NF-kB通路的参与.
- 暴露后,THP-1细胞显示出快速和升高的IL-1β水平,表明NLRP3炎症酶激活.
结论:
- 空气中的微塑料和纳米塑料,特别是氧化形式,会触发肺细胞中的无菌炎症.
- 塑料颗粒激活关键的炎症途径,包括NF-kB和NLRP3炎症体,从而导致肺病原体.
- 这些发现强调了通过吸入暴露于微型和纳米塑料的潜在健康风险.
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