Article ID Journal Published Year Pages File Type
4211840 Respiratory Medicine 2007 9 Pages PDF
Abstract

SummaryBackgroundEmphysema induced by cigarette smoking is characterized by an inflammatory process, which is resistant to steroid and remains active in lung tissue long after smoking has stopped. Latent adenoviral infection (Ad5) increases emphysema development and the inflammatory response to cigarette smoke and, in allergic lung inflammation, suppresses anti-inflammatory effects of steroids.ObjectivesThe present study was designed to examine the effect of smoking cessation and steroid treatment on lung emphysema and inflammation in a guinea pig model of emphysema and to determine if latent adenoviral infection induces resistance to the inflammatory effects of steroid.MethodsLatent adenovirus or sham infected animals exposed to room air or cigarette smoke for 16 weeks were either sacrificed immediately or treated with dexamethasone or diluent for an additional 5 weeks without smoke exposure. Lung morphometry, inflammatory cells and mediators were studied.ResultsSmoking cessation was associated with an increase in lung surface area and surface area to volume ratio. Smoking cessation was also associated with decreases in lung neutrophils, CD4 cells, and IL-8, RANTES and IFN-γ mRNAs to control levels. Steroid treatment significantly lowered neutrophils, eosinophils and IFN-γ mRNA and, while adenoviral infection did not alter these steroid-induced changes, it independently increased airway wall neutrophils and CD8 cells.Conclusionsmoking cessation decreases lung inflammation and latent adenoviral infection does not induce steroid resistance in this animal model.

Related Topics
Health Sciences Medicine and Dentistry Pulmonary and Respiratory Medicine
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