祖母过敏原敏感化重新编程了第二代后代对过敏原的表观遗传和呼吸道反应
Katie M Lebold1, Madeline Cook2, Alexandra B Pincus2
1Department of Emergency Medicine, Stanford University School of Medicine, Palo Alto, California, United States.
概括
在怀孕期间祖母暴露于过敏原会改变后代的DNA甲基化,增加喘风险. 这种在第二代的表观遗传重编程增强了对过敏原的呼吸道过敏反应.
科学领域:
- 环境表观遗传学环境表观遗传学
- 免疫学 免疫学 免疫学
- 发育生物学是发展生物学.
背景情况:
- 喘风险受环境,遗传和表观遗传因素的影响.
- DNA甲基化是一种表观遗传修饰,调节基因表达,并受到环境暴露的影响.
- 怀孕期间母亲喘会增加后代喘风险,但跨代表观遗传效应尚未完全理解.
研究的目的:
- 调查怀孕期间祖母家庭粉尘虫 (HDM) 过敏原敏感化对第二代小鼠呼吸道生理学和DNA甲基化的影响.
- 确定祖母对过敏原的暴露如何影响后代的表观遗传轨迹和过敏原反应.
主要方法:
- 在怀孕期间祖母暴露于HDM过敏原或载体后,研究了第二代小鼠.
- 气道生理学 (过敏反应) 和组织特异性DNA甲基化被评估在HDM敏感和过敏原原原始的第二代小鼠中.
- 基因表达分析针对与表观遗传修饰相关的途径,包括Smad3.
主要成果:
- 暴露于过敏原和车辆的祖母的后代在HDM敏感化后表现出呼吸道过敏反应.
- 祖母过敏原敏感性显著增强了呼吸道过敏反应,并在第二代后代中改变了表观基因组轨迹.
- 与表观遗传修饰相关的特定生物过程和信号通路在各个谱系之间存在差异,并指出Smad3失调.
结论:
- 在怀孕期间祖母对过敏原的暴露在第二代后代中建立了独特的表观遗传轨迹.
- 这种表观遗传重编程会影响过敏原反应,并可能导致跨世代的喘易感性.
- 这些发现为母亲喘如何影响遗传喘风险提供了潜在的机制.
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