Evidence establishing a link between prenatal and early-life stress and asthma development.
Evidence establishing a link between prenatal and early-life stress and asthma development.
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DOI：
10.1097/aci.0000000000000421
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发表时间：
2018-04
影响因子：
2.8
通讯作者：
Wright RJ
中科院分区：
文献类型：
--
作者：
Rosa MJ;Lee AG;Wright RJ
本次审查的目的是提供一个更新的理解不断变化的压力在怀孕期间和早期发展的哮喘相关表型的发病在儿童期，青春期和成年早期的影响。过去二十年来积累的证据已经确定，产前和早期生活中的心理压力和压力相关（例如，母亲焦虑或抑郁）增加儿童呼吸系统疾病的风险。最近的系统性综述和荟萃分析，包括许多前瞻性流行病学和病例对照研究证实了产前压力和儿童早期压力对喘息、哮喘和其他特应性相关疾病（湿疹和过敏性鼻炎）的发展有显著影响，许多研究显示了一种因果关系。两种性别的后代都容易受到围产期压力，但影响不同。压力对儿童喘息/哮喘的影响也可以通过暴露时间来改变。共同暴露于产前压力可以增强化学压力源的影响，如产前交通相关的空气污染，对儿童呼吸道疾病的风险。了解暴露剂量、时间、儿童性别和并发环境暴露之间的复杂相互作用，有望更全面地描述压力效应并确定易感亚组。虽然围产期压力和儿童哮喘相关表型之间的联系现在已经很好地建立，但压力使儿童易患慢性呼吸系统疾病的途径还没有很好地描述。喘息/哮喘和肺生长发育的病理生理学的中心机制重叠，涉及一系列事件，包括免疫、神经内分泌和自主神经功能以及氧化应激的破坏。在发育过程中，这些整合系统的稳态功能改变可以增强对哮喘的易感性和肺发育的改变。机制研究，更全面地评估生物标志物反映这些相互关联的压力反应系统和相关的监管过程中的变化，在孕妇和幼儿，可能是非常有益的。利用高通量系统范围的技术，包括表观基因组学（例如，需要DNA甲基化、microRNA、转录组学和微生物组学以及整合的多组学来推进这一科学领域。了解在脆弱的生命周期中发生的导致慢性呼吸道疾病风险的压力引起的生理变化可能会导致预防策略和可能的治疗干预措施的发展。
The objectives of this review is to provide an update on our evolving understanding of the effects of stress in pregnancy and during earlier development on the onset of asthma-related phenotypes across childhood, adolescence and into early adulthood. Accumulating evidence over the past two decades has established that prenatal and early life psychological stress and stress correlates (e.g., maternal anxiety or depression) increase the risk for childhood respiratory disorders. Recent systematic reviews and meta-analyses including numerous prospective epidemiological and case-control studies substantiate a significant effect of prenatal stress and stress in early childhood on the development of wheeze, asthma and other atopic-related disorders (eczema and allergic rhinitis), with many studies showing an exposure-response relationship. Offspring of both sexes are susceptible to perinatal stress, but effects differ. The impact of stress on child wheeze/asthma can also be modified by exposure timing. Co-exposure to prenatal stress can enhance the effect of chemical stressors, such as prenatal traffic-related air pollution, on childhood respiratory disease risk. Understanding complex interactions among exposure dose, timing, child sex, and concurrent environmental exposures promises to more fully characterize stress effects and identify susceptible subgroups. While the link between perinatal stress and childhood asthma related phenotypes is now well established, pathways by which stress predisposes children to chronic respiratory disorders are not as well delineated. Mechanisms central to the pathophysiology of wheeze/asthma and lung growth and development overlap and involve a cascade of events that include disrupted immune, neuroendocrine and autonomic function as well as oxidative stress. Altered homeostatic functioning of these integrated systems during development can enhance vulnerability to asthma and altered lung development. Mechanistic studies that more comprehensively assess biomarkers reflecting alterations across these interrelated stress response systems and associated regulatory processes, in both pregnant women and young children, could be highly informative. Leveraging high-throughput systems-wide technologies to include epigenomics (e.g., DNA methylation, microRNAs), transcriptomics, and microbiomics as well as integrated multi-omics are needed to advance this field of science. Understanding stress-induced physiological changes occurring during vulnerable life periods that contribute to chronic respiratory disease risk could lead to the development of preventative strategies and possible therapeutic interventions.