PM2.5通过影响肺部的HBD1表达而增加细菌入侵
Tianqi Zheng1, Yajun Wang1, Zheng Zhou1
1Department of Pulmonary and Critical Care Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Journal of immunology research
|February 5, 2024
概括
微粒颗粒物 (PM2.5) 暴露会通过降低人类β-防御素1 (HBD1) 水平而使Pseudomonas aeruginosa感染恶化. 补充HBD1或抑制MAPK/NF-κB通路可以减轻这些感染风险.
科学领域:
- 环境健康 环境健康
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
背景情况:
- 细颗粒物 (PM2.5) 是一个与感染风险增加相关的重要环境污染物.
- 人类β-防御素1 (HBD1) 是呼吸道上皮质的粘膜免疫的关键.
研究的目的:
- 调查PM2.5暴露对HBD1表达的影响及其在Pseudomonas aeruginosa感染中的作用.
- 阐明PM2.5引起的感染易感性所涉及的分子通路.
主要方法:
- 使用C57BL/6J小鼠和人类支气管上皮细胞 (HBE).
- 在PM2.5暴露和P. aeruginosa感染后评估HBD1表达 (mRNA和蛋白质).
- 检查了外源性HBD1管理和途径抑制剂 (MAPK,NF-κB) 的影响.
主要成果:
- 暴露在PM2.5下降了HBD1的表达,并增加了P. aeruginosa在HBE细胞和小鼠中的入侵.
- 联合PM2.5和P. aeruginosa暴露减少了小鼠的存活率.
- 外源性HBD1给药和途径抑制改善了PM2.5诱导的有害影响.
结论:
- 暴露于PM2.5会通过通过MAPK和NF-κB通路抑制HBD1表达而加剧P. aeruginosa感染.
- 外源性HBD1提供了针对PM2.5相关的肺部感染的潜在治疗策略.
- 这些发现为PM2.5相关的呼吸道感染的致病性提供了洞察力.
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