Mouse models to unravel the role of inhaled pollutants on allergic sensitization and airway inflammation
1 Laboratory for Translational Research in Obstructive Pulmonary Diseases, Department of Respiratory Medicine, Ghent University Hospital, De Pintelaan 185, 9000 Ghent, Belgium
2 Laboratory of Tumours and Developmental Biology, GIGA-research, University of Liège and CHU of Liège, Liège, Belgium
3 Department of Pneumology, GIGA-research, University of Liège and CHU of Liège, Liège, Belgium
4 Laboratory of Pneumology, Research Unit of Lung Toxicology, K.U.Leuven, Leuven, Belgium
Respiratory Research 2010, 11:7 doi:10.1186/1465-9921-11-7Published: 21 January 2010
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.