DNA甲基化:在空气污染暴露和喘控制之间是一个潜在的调解者
My-Nhi Nguyen1, Katelyn Queen2, Frank D Gilliland2
1Department of Population and Public Health Sciences, University of Southern California, Los Angeles, CA, USA. ngocmynh@usc.edu.
暴露于空气污染,特别是短期的PM10,与较差的喘控制有关. 血液细胞中的DNA甲基化变化可能会调解这种关系,从而提供有关喘病理生理学的见解.
科学领域:
- 环境表观遗传学环境表观遗传学
- 呼吸系统医学 呼吸系统医学
- 分子流行病学分子流行病学
背景情况:
- 空气污染是已知的喘恶化因素,其中涉及DNA甲基化 (DNAm) 的机制被假设.
- 了解空气污染等环境暴露如何通过表观遗传修饰影响喘控制至关重要.
研究的目的:
- 调查空气污染暴露与外周血液和T细胞中的DNAm之间的关联.
- 探索DNAm在空气污染和喘控制之间的关系中的潜在调解作用.
主要方法:
- 在651名暴露于各种空气污染物 (NO2,PM2.5,PM10,O3,EC,NOx) 的喘患者上进行了表观基因组广泛关联研究 (EWAS).
- 使用喘控制测试 (ACT) 成绩评估喘控制.
- 在全血和CD4+天真T细胞中使用Infinium HumanMethylation450 BeadChip阵列量化DNAm.
- 使用因果推理测试 (CIT) 来分析DNAm的调解.
主要成果:
- 短期的PM10暴露与降低喘控制相关.
- 鉴定了与PM10,EC,NOx (全血) 和PM10,NO2,PM2.5 (CD4+细胞) 相关的显著DNAm变化.
- 特定的CpG地点 (例如,cg04605532,cg10022248) 与空气污染暴露和喘控制有关.
- CIT分析表明,两个CpG位点 (cg02324789,cg10758278) 可能会调解PM10对喘控制的影响.
结论:
- 空气污染引起的DNA甲基化变化可能会影响特定位置的喘控制.
- 这些表观遗传变化为了解与空气污染相关的喘病理学提供了潜在的目标.
- 需要进一步的研究来证实因果关系,并阐明空气污染,DNA甲基化和喘之间的复杂相互作用.
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