Repair of airway epithelial injury and resolution of inflammation are highly regulated
processes. Inefficient clearance of apoptotic cells (efferocytosis) has the potential to cause an
accumulation of apoptotic material and the subsequent development of secondary necrosis and
perpetuation of chronic inflammation. Alveolar macrophages have the major role in effectively
clearing excess apoptotic cells in the airway. Several studies have identified defective efferocytosis
in the airways of subjects with chronic pulmonary diseases including chronic obstructive pulmonary
disease (COPD), asthma, lung cancer and cystic fibrosis. These defects have been shown to at least
partially relate to reduced levels of soluble mediators including mannose binding lectin (MBL) and
collectins (surfactant proteins A and D), as well as dysregulated expression of various macrophage
surface receptors and molecular pathways. These defects in macrophage function are potential
targets for new therapeutic interventions for chronic lung diseases.
Keywords: Alveolar macrophage, apoptosis, phagocytosis, efferocytosis, chronic lung disease, COPD.
