The HRCT scan pursuing real life pathology

The pathogenesis of chronic obstructive pulmonary disease (COPD) is widely considered to be the result of uncontrolled pulmonary inflammation. This is based on the original concept of a protease/antiprotease imbalance leading to peripheral tissue destruction and the development of emphysema. The premature development of emphysema in α₁-antitrypsin deficiency gave rise to this hypothesis and led to an increasing field of research in the 1970s investigating the inflammation in emphysema using bronchoalveolar lavage. In addition, a series of in vitro experiments investigated the ability of enzymes to produce emphysema-like lesions and its prevention by proteinase inhibitors.¹ More recently the smoking mouse and a series of gene knock-out and transgenic animals has explored not only the role of proteinases and inflammatory cells, but also proinflammatory cytokines, adhesion molecules, and growth factors in the development of emphysema.²

The study of upper airway secretions has indicated that inflammation is also present at this site, and several studies have demonstrated a proteinase/antiproteinase imbalance^3,4 that is likely to influence the nature of airways disease, including development of bronchiectasis, mucus hypersecretion, and disturbances of mucociliary clearance.⁵ However, many patients do not expectorate spontaneously, and hence the process of sputum induction was applied to obtain samples from the upper airways in patients with COPD, as defined by the presence of airways obstruction. These studies have led to a change in direction concerning the important cellular and inflammatory proteins that are key to the pathogenesis of …