臭氧和PM2.5暴露的气道转录组网络揭示了患有喘的儿童不同的关键驱动因素
Yoojin Chun1, Haritz Irizar2, Lingdi Zhang1
1Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Genome medicine
|December 23, 2025
概括
与健康儿童相比,患有喘的儿童在应对空气污染 (臭氧和PM2.5) 时表现出不同的呼吸道基因表达模式. 这些发现突出了污染引发的喘恶化治疗的潜在新目标.
科学领域:
- 环境健康 环境健康
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
背景情况:
- 空气污染,包括臭氧和细颗粒物 (PM2.5),加剧了喘,导致发病率增加.
- 了解空气污染对呼吸道影响的分子机制对于开发有效干预措施至关重要.
- 喘是一种慢性呼吸道疾病,不成比例地影响儿童,并对公共卫生产生重大影响.
研究的目的:
- 在暴露于臭氧和PM2.5.5后,研究患有喘和没有喘的儿童之间呼吸道转录组网络的差异.
- 在这些网络中识别与污染物暴露相关的关键驱动基因.
- 探索已识别的关键驱动因素与气道中的细胞炎症标志物之间的关系.
主要方法:
- 从纽约大都会地区招募了307名儿童 (167名患有喘,140名没有).
- 绘制单个空气污染物 (臭氧和PM2.5) 暴露的地图,并采集鼻腔和支气管样本.
- 应用因果网络构建和关键驱动器分析到转录组数据.
主要成果:
- 在患有喘和没有喘的儿童中,确定了臭氧和PM2.5暴露的明显的呼吸道因果网络.
- 在患有喘的儿童中,网络与亲炎性自适应性免疫过程有关,特定的关键驱动因素被确定为臭氧 (例如,CLC,CPA3) 和PM2.5 (例如,TNFRSF10C).
- 在健康儿童中,臭氧网络的关键驱动因素与DNA修复和免疫调节有关,与喘组形成鲜明对比.
结论:
- 在患有喘和没有喘的儿童之间,呼吸道转录组对臭氧和PM2.5的反应存在显著差异.
- 已确定的关键驱动基因代表了减轻空气污染对喘影响的潜在治疗点.
- 这些发现为了解污染物加重喘和制定个性化治疗策略提供了分子基础.
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