Air Pollution Exposure Impairs Airway Epithelium IFN-β Expression in Pre-School Children.
Matteo Bonato, Elisa Gallo, Martina Turrin, Erica Bazzan, Federico Baraldi, Marina Saetta, Dario Gregori, Alberto Papi, Marco Contoli, Simonetta Baraldo
Author Information
Matteo Bonato: Respiratory Diseases Clinic, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, Padova, Italy.
Elisa Gallo: Unit of Biostatistics, Epidemiology and Public Health, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, Padova, Italy.
Martina Turrin: Respiratory Diseases Clinic, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, Padova, Italy.
Erica Bazzan: Respiratory Diseases Clinic, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, Padova, Italy.
Federico Baraldi: Respiratory Section, Department of Translational Medicine, University of Ferrara, Ferrara, Italy.
Marina Saetta: Respiratory Diseases Clinic, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, Padova, Italy.
Dario Gregori: Unit of Biostatistics, Epidemiology and Public Health, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, Padova, Italy.
Alberto Papi: Respiratory Section, Department of Translational Medicine, University of Ferrara, Ferrara, Italy.
Marco Contoli: Respiratory Section, Department of Translational Medicine, University of Ferrara, Ferrara, Italy.
Simonetta Baraldo: Respiratory Diseases Clinic, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, Padova, Italy.
Introduction: Air pollution is a risk factor for respiratory infections and asthma exacerbations. We previously reported impaired Type-I and Type-III interferons (IFN-β/λ) from airway epithelial cells of preschool children with asthma and/or atopy. In this study we analyzed the association between rhinovirus-induced IFN-β/λ epithelial expression and acute exposure to the principal outdoor air pollutants in the same cohort. Methods: We studied 34 children (17asthmatics/17non-asthmatics) undergoing fiberoptic bronchoscopy for clinical indications. Bronchial epithelial cells were harvested by brushing, cultured and experimentally infected with Rhinovirus Type 16 (RV16). RV16-induced IFN-β and λ expression was measured by quantitative real time PCR, as was RV16vRNA. The association between IFNs and the mean exposure to PM10, SO2 and NO in the day preceding bronchoscopy was evaluated using a Generalized Linear Model (GLM) with Gamma distribution. Results: Acute exposure to PM10 and NO was negatively associated to RV16-induced IFNβ mRNA. For each increase of 1ug/m of NO we found a significative decrease of 2.3x10 IFN-β mRNA copies and for each increase of 1ug/m of PM10 a significative decrease of 1x10 IFN-β mRNA copies. No significant associations were detected between IFN-λ mRNA and NO nor PM10. Increasing levels of NO (but not PM10) were found to be associated to increased RV16 replication. Conclusions: Short-term exposure to high levels of NO and PM10 is associated to a reduced IFN-β expression by the airway epithelium, which may lead to increased viral replication. These findings suggest a potential mechanism underlying the link between air pollution, viral infections and asthma exacerbations.
