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The Proceedings of the American Thoracic Society 2:361-366 (2005)
© 2005 The American Thoracic Society

Mechanisms and Experimental Models of Chronic Obstructive Pulmonary Disease Exacerbations

Patrick Mallia and Sebastian L. Johnston

Department of Respiratory Medicine, National Heart and Lung Institute, Imperial College London, London, United Kingdom

Correspondence and requests for reprints should be addressed to Sebastian L. Johnston, M.B., B.S., Ph.D., F.R.C.P., Department of Respiratory Medicine, National Heart and Lung Institute, Imperial College London, Norfolk Place, London W2 1PG, UK. E-mail: s.johnston{at}ic.ac.uk

Exacerbations of chronic obstructive pulmonary disease (COPD) are a major cause of morbidity, mortality, and rising health care costs. In addition, they are associated with an accelerated loss of lung function and thus have a direct effect on disease progression. There are few studies examining the cellular and molecular mechanisms of COPD exacerbations. Exacerbations are linked to increased airway inflammation and oxidative stress, but many questions remain unanswered regarding the key inflammatory cells and mediators. Current therapies for COPD exacerbations are of limited effectiveness, and a better understanding of the inflammatory events at exacerbation is required to devise new therapeutic agents. The development of experimental models of exacerbation—for example, the use of experimental rhinovirus infection in humans with COPD—would greatly facilitate studies of exacerbations.

Key Words: chronic obstructive pulmonary disease • acute exacerbations • virus infection




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