在喘的3D呼吸模型中评估对多环芳化合物毒性的敏感性
Reese M Valdez1,2, Brianna N Rivera1,2, Yvonne Chang1,2
1Environmental and Molecular Toxicology Department, Oregon State University, Corvallis, OR, United States.
Frontiers in toxicology
|May 6, 2024
概括
炎症,就像在喘中看到的炎症一样,显著加剧了由多环芳 (PAHs) 引起的肺细胞损伤. 这项研究表明,先前存在的肺炎会增加对吸入污染物的敏感性,影响公共健康.
科学领域:
- 环境健康 环境健康
- 毒理学 毒理学 毒理学
- 肺部医学 肺部医学
背景情况:
- 化学和非化学压力因素的累积风险对公共健康至关重要.
- 肺炎可能会改变肺部的化学毒性,但机制尚不清楚.
研究的目的:
- 评估炎症如何影响人类支气管细胞中的多环芳 (PAHs) 毒性.
- 为了研究先前存在的肺炎和吸入污染物暴露之间的相互作用.
主要方法:
- 初级人类支气管上皮细胞 (HBEC) 在空气-液体界面 (ALI) 培养.
- 细胞与IL-13分化,以模仿一种类似喘的表型.
- 细胞暴露于甲 (BAP),并分析了细胞毒性,屏障完整性和基因表达.
主要成果:
- 与正常细胞相比,受IL-13治疗的细胞在暴露于BAP时显著降低了屏障完整性.
- 在IL-13表型细胞中,BAP暴露诱导了屏障完整性,粘液产生和炎症标志物的剂量依赖性变化.
- 在BAP暴露后,RNA测序表明IL-13表型细胞的增殖潜力增加和免疫反应降低.
结论:
- 这项研究提供了第一个人体体外试验证据,表明先前存在的肺炎会加剧PAH暴露的肺毒性.
- 研究结果强调了在评估肺部疾病风险时考虑环境因素的重要性.
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