聚烯纳米塑料通过EGFR/ERK依赖的肺上皮屏障功能障碍加剧了室内灰尘虫诱导的过敏呼吸道炎症
Qing Wang1, Wen He1, Yufeng Zhou2
1Department of Respiratory Medicine, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai 201102, China.
Ecotoxicology and environmental safety
|May 17, 2025
概括
空气中的聚乙烯纳米颗粒 (PS-NP) 通过破坏肺上皮屏障,使过敏性喘恶化. 这种恶化与表皮生长因子受体 (EGFR) 途径有关,突出了呼吸系统健康风险的关键机制.
科学领域:
- 环境健康 环境健康
- 毒理学 毒理学 毒理学
- 呼吸系统医学 呼吸系统医学
背景情况:
- 空气中的微型和纳米塑料 (MNP) 引发了对呼吸系统健康的担忧.
- 对于MNP对过敏性喘的具体影响尚不清楚.
研究的目的:
- 研究聚乙烯纳米颗粒 (PS-NP) 如何影响过敏喘.
- 探索PS-NPs诱导的肺上皮质屏障功能障碍背后的机制.
主要方法:
- 使用室内灰尘 (HDM) 和暴露于PS-NPs的小鼠创建了一种过敏喘模型.
- 在体外研究中使用小鼠肺上皮细胞 (MLE-12) 和A549细胞来评估PS-NP的影响.
- 转录组测序和EGFR通路抑制 (AG1478) 用于确定分子机制.
主要成果:
- 暴露于PS-NPs显著加剧了小鼠的过敏性喘,增加了呼吸道炎症和Th2-介导反应 (IL-4,IL-13,IgE,乙氨基酸).
- 在膜区域积聚PS-NP,导致肺上皮质屏障功能障碍,特别是在HDM敏感化时.
- 表皮生长因子受体 (EGFR) / 细胞外调节激酶 (ERK) 途径被确定为PS-NP诱导的肺屏障损伤和喘恶化中的关键调解者.
结论:
- 聚乙烯纳米颗粒通过EGFR/ERK通路损害肺上皮质屏障完整性,从而加剧过敏性喘.
- 了解这些分子机制对于评估与空气中纳米塑料相关的健康风险至关重要.
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