• M Roth.
• Department of Molecular Medicine, Woolcock Institute for Medical Research, Camperdown, New South Wales, Australia. Michaelr@med.usyd.edu.au
• Int. J. Tuberc. Lung Dis. 2008 Apr 1; 12 (4): 375-80.

AbstractChronic obstructive pulmonary disease (COPD) is mostly caused by cigarette smoking and affects up to 25% of smokers. Air pollution and occupational exposure to dust and fumes can also induce COPD. COPD is characterised by airflow limitation that is not fully reversible and chronic inflammation of the lung. Most patients with COPD also have evidence of tissue remodelling in the smaller airways. How the different pathological features are linked remains unknown. The inflammation of the COPD lung is initially caused by cigarette smoke and the increased infiltration of immune cells into the lung, but it is not clear why the inflammation persists after smoking cessation, while other pathologies partly reverse. Furthermore, anti-inflammatory treatments are not very successful and only control the symptoms but do not cure the disease. Animal models suggest that the imbalance of proteases and antiproteases is central to the major pathologies in the COPD lung. However, this hypothesis was never fully confirmed in humans and may only explain the degenerative stage of the disease, emphysema. The role of tissue-forming cells in the pathogenesis of COPD has not been adequately studied and indicates a deregulated synthesis of growth factors and cytokines in COPD. Finally, recent studies indicate that alpha-1-antitrypsin activity plays a role in all forms of COPD.

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