Figure 1.

Mechanisms underlying COPD development. Multiple risk factors including cigarette smoke and other irritants activate alveolar macrophages and epithelial cells in the respiratory tract leading oxidative stress followed release of multiple inflammatory mediators. These inflammatory mediators, particularly chemokines, attract neutrophils and monocytes as well as T helper cells. The activated alveolar macrophages and epithelial cells also release proteases such as neutrophil elastase and matrix metalloproteinase 9 (MMP-9), which damage the lung parenchyma resulting in lung vascular remodeling, alveolar wall destruction and mucus hypersecretion. In addition, the activated macrophages and epithelial cells release fibrogenic mediators, such as TGFβ which causes EMT and eventually small airway fibrosis.

Abbreviations: COPD, chronic obstructive pulmonary disease; EMT, epithelial-mesenchymal transition.