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* From the Department of Thoracic Medicine, National Heart and Lung Institute, London, UK.
Correspondence to: Peter J. Barnes MA, DM, DSc, Department of Thoracic Medicine, National Heart and Lung Institute, Dovehouse St, London SW3 6LY, UK;
Although considerable progress has been made in understanding the cellular and molecular mechanisms of asthma, much less attention has been paid to COPD. The inflammatory process in COPD is very different from that in asthma, with different inflammatory cells, mediators, inflammatory effects, and response to therapy. Airway inflammation in asthma, characterized by an eosinophilic inflammation affecting all the airways but not lung parenchyma, is linked to airway hyperresponsiveness. In COPD, there is a predominantly neutrophilic inflammation in the airways. Parenchymal destruction is an important irreversible feature and leads to airflow obstruction through dynamic compression. The eosinophilic inflammation in asthma is markedly suppressed by corticosteroids, but they have no appreciable effect on the inflammation in COPD, consistent with a failure of long-term corticosteroids to alter the progression of COPD.
Key Words: antiprotease • corticosteroids • eosinophil • macrophage • matrix metalloprotinase • neutrophil • neutrophil elastase • protease
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