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对PM_2.5暴露的遗传易感性和儿科喘中的转录反应:从单细胞转录组学的见解

Jelte Kelchtermans^1,2, Huiqi Qu¹, Cuiping Hou¹

¹Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, PA, United States.

Frontiers in immunology

|February 19, 2026

概括

遗传变异影响儿童喘中的微粒颗粒物 (PM2.5) 敏感性,涉及TGF-β1信号传递. 这项研究确定了喘儿童PM2.5易受性的潜在分子途径.

科学领域:

基因组学就是基因组学.
免疫学免疫学免疫学
环境健康环境健康

背景情况:

暴露于细颗粒物 (PM2.5) 加剧了儿童喘,降低了治疗的有效性.
儿童喘中PM2.5敏感性的分子机制在很大程度上是未知的.
对于PM2.5敏感性的多基因风险评分 (sPRS) 与喘严重程度相关.

研究的目的:

确定与PM2.5敏感性相关的遗传变异相关的生物途径和调节者.
调查高sPRS的儿童是否表现出免疫转录模式,表明PM2.5易感性增加.

主要方法:

与sPRS变异相关的基因被分析为途径和转录因子丰富.
单细胞RNA测序分析了患有高和低sPRS的儿童的免疫细胞.
对免疫细胞进行了差异性基因表达和通路分析.

主要成果:

与sPRS相关的基因显示了SMAD2/3和MAPK信号的丰富,表明TGF-β1通路参与.
途径分析显示,免疫细胞的炎症和应激反应途径得到了丰富.
Perturbagen 分析确定了 TGF-β1 通路调节者.

结论:

综合性分析表明,TGF-β1-SMAD/MAPK信号传递是儿童喘中对PM2.5遗传敏感性的关键途径.
发现是产生假设的,需要进一步的功能验证.
这项研究为了解环境喘触发因素的遗传贡献提供了基础.

关键词:

对于PM2.5来说,这是一个很好的例子.喘喘是一种基因与环境的相互作用.单细胞转录组学单细胞转录组学易感性易感性易感性

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