Adenoviral E1A modulates inflammatory mediator expression by lung epithelial cells exposed to PM10 |
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Authors: | Fujii Takeshi Hogg James C Keicho Naoto Vincent Renaud Van Eeden Stephan F Hayashi Shizu |
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Affiliation: | McDonald Research Laboratory and iCAPTURE Center, University of British Columbia, St. Paul's Hospital, 1081 Burrard Street, Vancouver, British Columbia V6Z 1Y6, Canada. |
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Abstract: | We examined the hypothesis that ambient particulate matter with a diameter of <10 microm (PM(10))-induced lung inflammation is amplified by latent adenovirus infection. Inflammatory mediator expression in response to PM(10) exposure was compared between adenovirus E1A-transfected A549 alveolar epithelial cells and cells transfected with control plasmid. Messenger RNA was measured by the RNase protection assay and protein by ELISA or immunocytochemistry. Intercellular adhesion molecule-1 and IL-8 mRNA and protein were increased in E1A-positive cells exposed to 500 microg/ml PM(10). Monocyte chemoattractant protein-1 mRNA and protein were unchanged in E1A-positive cells but increased in E1A-negative cells after 100 and 500 microg/ml PM(10) exposure. Electrophoretic mobility shift assays showed increased NF-kappaB and decreased specificity protein 1 nuclear binding in E1A-positive cells exposed to PM(10). These results indicate that E1A modulates cytokine and adhesion molecule expression in epithelial cells in a manner that could amplify PM(10)-induced lung inflammation. We suggest that this amplified inflammatory response may contribute to the pathogenesis of exacerbations of chronic obstructive pulmonary disease associated with exposure to particulate matter air pollution. |
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