Mouse models to unravel the role of inhaled pollutants on allergic sensitization and airway inflammation.
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.
Maes
Tania
T
Laboratory for Translational Research in Obstructive Pulmonary Diseases, Department of Respiratory Medicine, Ghent University Hospital, De Pintelaan 185, 9000 Ghent, Belgium. tania.maes@ugent.be
Provoost
Sharen
S
Lanckacker
Ellen A
EA
Cataldo
Didier D
DD
Vanoirbeek
Jeroen A J
JA
Nemery
Benoit
B
Tournoy
Kurt G
KG
Joos
Guy F
GF
D000280:Administration, Inhalation; D000818:Animals; D004195:Disease Models, Animal; D006801:Humans; D008168:Lung / Q000187:drug effects*; D051379:Mice; D052638:Particulate Matter / Q000008:administration & dosage / Q000633:toxicity*; D011014:Pneumonia / Q000139:chemically induced* / Q000503:physiopathology*; D012130:Respiratory Hypersensitivity / Q000139:chemically induced* / Q000503:physiopathology*
D052638:Particulate Matter