Remodelling of peripheral lung tissue in COPD

Chronic obstructive pulmonary disease (COPD) is a major worldwide public health problem caused by the inhalation of toxic particles and gases primarily as a result of tobacco smoking 1. In 2001, the Global Initiative for Chronic Obstructive Lung Disease (GOLD) assembled an international panel of experts to develop, continuously monitor and upgrade guidelines for diagnosis of the disease, classification of its severity and the optimum management of COPD 1, 2. The criteria for diagnosis and severity of COPD are based on measurement of post-bronchodilator forced expiratory volume in one second (FEV1) and its ratio to forced vital capacity (FVC) 1, 2. Because these measurements reflect the time constant for lung emptying, they detect the combined effect of resistance offered by the airways and lung compliance, which determines the elastic force required to drive air out of the lungs. However, these measurements cannot separate one from the other. The lesions at both the site of airway obstruction and emphysematous destruction contain a persistent infiltration of inflammatory immune cells that becomes more extensive and severe as COPD progresses 3–6. This inflammatory immune response is inextricably linked to a repair and remodelling process that thickens the walls and narrows the lumen of small conducting airways and causes emphysematous destruction of gas-exchanging tissue 6, 7. Although the lungs from most patients with COPD have a mixture of lesions, studies based on high-resolution computed tomography indicate that they can be separated into phenotypes in which either airway obstruction or emphysematous destruction predominate 8, 9. In the current issue of the European Respiratory Journal , Black et al. 10 provide new information concerning the elastin …