Gene-air pollution interactions in asthma.
Gene-air pollution interactions in asthma.
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DOI：
10.1513/pats.200701-031aw
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发表时间：
2007-07-01
期刊：
影响因子：
--
通讯作者：
London, Stephanie J
中科院分区：
文献类型：
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作者：
London, Stephanie J
遗传和环境因素相互作用导致哮喘。然而，基因研究普遍忽视了环境因素，环境研究也普遍忽视了遗传学。因此，很少有文献中有与哮喘相关的特定基因-环境相互作用的例子。吸入污染物的遗传相互作用最明显的例子是内毒素、环境烟草烟雾和臭氧。哮喘中的内毒素-遗传相互作用是本次会议另外两篇手稿的重点，因此这篇综述集中在环境烟草烟雾和臭氧上。在为数不多的文献中，有证据表明参与氧化应激的特定基因，特别是GSTM1和TNF，在对臭氧和环境烟草烟雾的呼吸反应中所起的作用。有关先天免疫途径的基因数据很少，先天免疫途径对内毒素的反应至关重要，可能在对臭氧和环境烟草烟雾的反应中发挥作用。参与氧化应激的基因可能与空气污染物和与哮喘表型有关的饮食相互作用。未来推动该领域发展的方向包括全基因组关联研究，更好地评估暴露和表型，以及考虑与饮食和其他影响个体易感性的辅助因素的联合作用。
Genetic and environmental factors interact to cause asthma. However, genetic studies have generally ignored environmental factors and environmental studies have generally ignored genetics. Thus, there are few examples from the literature of specific gene-environment interactions in relation to asthma. The clearest examples of genetic interactions for inhaled pollutants exist for endotoxin, environmental tobacco smoke, and ozone. Endotoxin-genetic interactions in asthma are the focus of two other manuscripts from this conference, so this review focuses on environmental tobacco smoke and ozone. In the sparse literature, there is evidence for the role of specific genes involved in oxidative stress, notably GSTM1 and TNF, in the respiratory responses to ozone and environmental tobacco smoke. There are few data on genes involved in innate immune pathways, which are crucial in response to endotoxin and may play a role in response to ozone and environmental tobacco smoke. Genes involved in oxidative stress may interact with both air pollutants and diet in relation to asthma phenotypes. Future directions to advance the field include whole genome association studies, better assessment of exposure and phenotypes, and consideration of joint interactions with diet and other co-factors that influence individual susceptibility.