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Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
Published on: August 25, 2017
[Childhood respiratory infection in the pathogenesis of COPD]
Masaki Ishii1, Shinji Teramoto
1Department of Geriatric Medicine, Graduate School of Medicine, The University of Tokyo.
Abstract:
A respiratory infection in childhood has been implicated in one of the risk factors for COPD. The hypothesis that latent adenoviral infection is involved in the pathogenesis of COPD have been studied for 15 years. A DNA virus, adenovirus(Ad), early gene 1A (ElA gene) was identified in lung tissue of COPD. The E1A gene expression enhances the soluble intercellular adhesion molecule (ICAM) 1 expression and the recruitment of inflammatory cells into airways of COPD lungs. In vitro experiments, E1A gene transfected cells exhibited the enhanced inflammatory response to tobacco smoke. The excess production of ICAM-1, IL-8, and TGF- beta by lung epithelial cells transfected with the Ad E1A gene. Respiratory infections in childhood including Ad infection may be an important risk factor for the pathogenesis of COPD.
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