Mouse models to unravel the role of inhaled pollutants on allergic sensitization and airway inflammation

• Published in: Respiratory research Vol. 11; no. 1; p. 7
• Main Authors: Maes, Tania, Provoost, Sharen, Lanckacker, Ellen A, Cataldo, Didier D, Vanoirbeek, Jeroen A J, Nemery, Benoit, Tournoy, Kurt G, Joos, Guy F
• Format: Journal Article Web Resource
• Language: English
• Published: England BioMed Central Ltd 21.01.2010; BioMed Central; BMC
• Subjects: Administration, Inhalation; Allergies; Animals; Asthma; Biochemistry, biophysics & molecular biology; Biochimie, biophysique & biologie moléculaire; Chronic illnesses; Cigarettes; Disease Models, Animal; Health aspects; Health risk assessment; Humans; Immunization; Life sciences; Lung - drug effects; Mice; Outdoor air quality; Particulate Matter - administration & dosage; Particulate Matter - toxicity; Pathogenesis; Pathology; Pneumonia - chemically induced; Pneumonia - physiopathology; Pollutants; Public health; Respiratory Hypersensitivity - chemically induced; Respiratory Hypersensitivity - physiopathology; Review; Risk factors; Sciences du vivant; Studies; Tobacco smoke; Belgium
• ISSN: 1465-993X; 1465-9921; 1465-993X; 1465-9921
• 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.