Figure 2.

Overview of the etiology and pathogenesis of COPD. Risk factors for the development of COPD include: cigarette smoke; air pollution; occupational exposures; childhood asthma; respiratory infections; and alpha 1-anti-trypsin (α1AT) deficiency. Upon exposure to inhaled toxicants, lung structural cells, including epithelial cells and fibroblasts, as well as alveolar macrophages, are activated. These cells produce inflammatory mediators to recruit additional inflammatory cells, such as neutrophils, macrophages, and lymphocytes, to the site of exposure. This augments the expression of inflammatory mediators, such as TNF-α, IL-6, CCL2, CCL7, CXCL1, CXCL5, CXCL8 (IL-8), LTB4, and COX-2, and releases proteases, such as NE, cathepsins, and MMPs. This cascade of events can lead to chronic pulmonary inflammation, airflow obstruction, and alveolar wall destruction (emphysema) in a susceptible individual. Created with BioRender.com.