Air pollution, bronchiolitis, and asthma: the role of nasal microRNAs.
Air pollution, bronchiolitis, and asthma: the role of nasal microRNAs.
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DOI：
10.1016/s2213-2600(22)00133-3
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发表时间：
2022-08
影响因子：
76.2
通讯作者：
Hasegawa, Kohei
中科院分区：
文献类型：
--
作者：
Makrinioti, Heidi;Camargo, Carlos A.;Zhu, Zhaozhong;Freishtat, Robert J.;Hasegawa, Kohei
严重的细支气管炎（即需要住院治疗的细支气管炎）给婴儿带来了巨大的急性护理负担，并导致慢性呼吸道后遗症，如反复喘息和哮喘。1越来越多的研究表明，在患有严重细支气管炎的婴儿中，环境暴露在哮喘的发展中起着至关重要的作用。来自观察性研究的数据显示，暴露于较高水平空气污染（例如，如果他们的出生住所靠近主要道路）的严重细支气管炎婴儿患哮喘的风险比暴露于较低水平空气污染的婴儿高1.2 - 1.6倍。2，3哮喘的表观遗传学研究引起了人们对检查表观遗传调节作为空气污染和哮喘之间联系的介导者的作用的兴趣。研究报告说，在应对空气污染暴露，鼻气道表观遗传过程驱动哮喘的发展。4基于RNA和非基于RNA的表观遗传机制，如microRNA转录后调节、DNA甲基化和组蛋白修饰，都与毛细支气管炎和哮喘的发病机制有关。然而，2019年的研究表明，DNA甲基化可能是基因表达变化的结果，而不是原因。5因此，在患有严重细支气管炎的婴儿中，基于RNA的表观遗传机制-主要是microRNA转录后调节-可以作为空气污染和哮喘之间联系的关键表观遗传介质。对这种RNA假说的研究是有吸引力的，因为鼻气道microRNA可用作严重细支气管炎婴儿（一个大的高危人群）的儿童哮喘的生物标志物和预防靶点。本评论讨论了当前的证据和知识差距，围绕鼻气道microRNA转录后调节作为严重毛细支气管炎婴儿空气污染暴露和哮喘发展途径中的关键介质的潜在作用。
Severe bronchiolitis (ie, bronchiolitis that requires hospitalisation) imposes a substantial acute care burden on infants and leads to chronic respiratory sequelae, such as recurrent wheeze and asthma. 1 An increasing number of studies show that, in infants with severe bronchiolitis, environmental exposures play an essential role in the development of asthma. Data from observational studies show that infants with severe bronchiolitis who are exposed to higher levels of air pollution (for example, if their birth residence is located close to a main road) have a 1· 2–1· 6 times higher risk of developing asthma than those exposed to lower levels of air pollution. 2, 3 Epigenetic studies of asthma create interest in examining the role of epigenetic regulation as a mediator of the link between air pollution and asthma. Research reports that, in response to air pollution exposure, nasal airway epigenetic processes drive asthma development. 4 Both RNA-based and non-RNA-based epigenetic mechanisms, such as microRNA post-transcriptional regulation, DNA methylation, and histone modification, are implicated in the pathogenesis of both bronchiolitis and asthma. However, research from 2019 suggests that DNA methylation could be a consequence of changes in gene expression, rather than a cause. 5 Therefore, among infants with severe bronchiolitis, RNA-based epigenetic mechanisms—mainly microRNA post-transcriptional regulation—could serve as key epigenetic mediators of the link between air pollution and asthma. Investigation of this RNA hypothesis is attractive, as nasal airway microRNAs could be used both as biomarkers and as preventive targets for childhood asthma in infants with severe bronchiolitis, a large and high risk population. This Comment discusses the current evidence and knowledge gaps around the potential role of nasal airway microRNA post-transcriptional regulation as a key mediator in the development pathway of air pollution exposure and asthma among infants with severe bronchiolitis.