Chronic obstructive pulmonary disease (COPD) is mainly caused by smoking and presents with shortness of breath that is progressive and irreversible. It is a worldwide health problem and the fourth most common cause of chronic disability and mortality, even in developed countries. It is a complex disease in which both the airway and lung parenchyma are involved. In this review we will be mainly focusing on the airway component of the disease. We have reviewed the current literature on airway inflammation and remodelling in smoking-related COPD. It is not only the tobacco smoking which can lead to chronic inflammation, but also the persistent presence of pathogenic microorganisms in the airways. Detailed data on these in COPD are sparse. One potential mechanism contributing to small airway fibrosis/obliteration and change in extracellular matrix is epithelial mesenchymal transition (EMT). When associated with angiogenesis (so called EMT-Type-3) it may well also be the link with the development of cancer, which is closely associated with COPD, predominantly in large airways. In this paper we focused on: 1) the role of inflammation in developing COPD; 2) recent observations on structural and cellular changes which might have relevance to a major feature of COPD that is poorly understood, namely, the striking vulnerability of patients with COPD to develop lung cancer; 3) the potential role of respiratory infections in COPD.
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