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Am J Physiol Lung Cell Mol Physiol (October 18, 2002). doi:10.1152/ajplung.00197.2002
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Articles in PresS, published online ahead of print October 18, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00197.2002
Submitted on June 19, 2002
Accepted on October 10, 2002

Adenoviral E1A modulates inflammatory mediator expression by lung epithelial cells exposed to PM10 -R1

Takeshi Fujii1, James C. Hogg1, Naoto Keicho1, Renaud Vincent2, Stephan F. van Eeden1, and Shizu Hayashi1*

1 McDonald Research Laboratory and iCAPTURE Center, University of British Columbia, Vanvcouver, British Columbia, Canada
2 Environmental Health Directorate, Health Canada, Ottawa, Ontario, Canada

* To whom correspondence should be addressed. E-mail: shayashi{at}mrl.ubc.ca.

We examined the hypothesis that ambient particulate matter (PM10) induced lung inflammation is amplified by latent adenovirus infection. Inflammatory mediator expression in response to PM10 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 interleukin-8 mRNA and protein were increased in E1A-positive cells exposed to 500 µg/ml PM10. Monocyte chemoattractant protein-1 mRNA and protein were unchanged in E1A-positive cells but increased in E1A-negative cells after 100 and 500 µg/ml PM10 exposure. Electrophoretic mobility shift assays showed increased nuclear factor-{kappa}B and decreased specificity protein 1 nuclear binding in E1A-positive cells exposed to PM10. These results indicate that E1A modulates cytokine and adhesion molecule expression in epithelial cells in a manner that could amplify PM10 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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