Models of Exacerbations in Asthma and COPD

Editor(s): Sjöbring U. (Lund) 
Taylor J.D. (Lund) 
Table of Contents
Vol. 14, No. , 2007
Section title: Animal COPD Models
Sjobring U, Taylor JD (eds): Models of Exacerbations in Asthma and COPD. Contrib Microbiol. Basel, Karger, 2007, vol 14, pp 113-125
Animal COPD Models

Animal Models of Cigarette Smoke-Induced Chronic Obstructive Lung Disease

Churg A. · Wright J.
Department of Pathology, University of British Columbia, Vancouver, B.C., Canada Sjobring U, Taylor JD (eds): Models of Exacerbations in Asthma and COPD. Contrib Microbiol. Basel, Karger, 2007, vol 14, pp 113-125 (DOI:10.1159/000107058)


Recent years have seen an explosion of animal models of cigarette smoke-induced chronic obstructive lung disease (COPD). Almost all of these have concentrated on the induction and prevention of emphysema. Neutrophils and neutrophil elastase, macrophages and macrophage-derived metalloproteases, lymphocytes, TNF-, and oxidants have all been shown to play a role in the pathogenesis of emphysema in animal models, and interventions using either knockout mice or drugs have indicated possible preventive/therapeutic avenues. There is less in the way of models of smoke-induced small airway remodeling and almost nothing is known of its pathogenesis. Cigarette smoke has been shown to induce vascular remodeling and pulmonary hypertension in laboratory animals, and these mechanisms are beginning to be understood. A major limitation of existing animal models is that most produce relatively mild disease (no more severe than corresponding to the GOLD 2 stage of human COPD), and none of the models show the smokeindependent progressive disease seen in humans with GOLD 3 or 4 COPD. There are no models of cigarette smoke-induced chronic bronchitis in animals and there are no models of acute exacerbations of COPD.

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