Laboratory for Translational Research in Obstructive Pulmonary Diseases, Department of Respiratory Medicine, Ghent University Hospital, De Pintelaan 185, 9000 Ghent, Belgium.
Respir Res. 2010 Jan 21;11(1):7. doi: 10.1186/1465-9921-11-7.
Air pollutant exposure has been linked to a rise in wheezing illnesses. Clinical data highlight that exposure to mainstream tobacco smoke (MS) and environmental tobacco smoke (ETS) as well as exposure to diesel exhaust particles (DEP) could promote allergic sensitization or aggravate symptoms of asthma, suggesting a role for these inhaled pollutants in the pathogenesis of asthma. Mouse models are a valuable tool to study the potential effects of these pollutants in the pathogenesis of asthma, with the opportunity to investigate their impact during processes leading to sensitization, acute inflammation and chronic disease. Mice allow us to perform mechanistic studies and to evaluate the importance of specific cell types in asthma pathogenesis. In this review, the major clinical effects of tobacco smoke and diesel exhaust exposure regarding to asthma development and progression are described. Clinical data are compared with findings from murine models of asthma and inhalable pollutant exposure. Moreover, the potential mechanisms by which both pollutants could aggravate asthma are discussed.
空气污染暴露与喘息性疾病的增加有关。临床数据突出表明，接触主流烟草烟雾（MS）和环境烟草烟雾（ETS）以及接触柴油废气颗粒（DEP）可促进过敏敏化或加重哮喘症状，表明这些吸入性污染物在哮喘发病机制中起作用。小鼠模型是研究这些污染物在哮喘发病机制中潜在作用的一种有价值的工具，有机会研究它们在致敏、急性炎症和慢性疾病发展过程中的影响。老鼠使我们能够进行机制研究，并评估特定细胞类型在哮喘发病机制中的重要性。在这篇综述中，描述了烟草烟雾和柴油废气暴露对哮喘发展和进展的主要临床影响。将临床数据与哮喘和可吸入污染物暴露的小鼠模型的研究结果进行了比较。此外，还讨论了这两种污染物加重哮喘的潜在机制。
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