The Effect of Colonization with Potentially Pathogenic Microorganisms on Efferocytosis in Chronic Obstructive Pulmonary Disease

To the Editor: Smoking cessation alone will not completely reverse the abnormal chronic airways inflammation in established chronic obstructive pulmonary disease (COPD). We have shown an abnormal accumulation of apoptotic bronchial epithelial cells (1) and impaired clearance of this apoptotic material (“efferocytosis”) by alveolar macrophages in both current and ex-smoker subjects with COPD and smokers (2) and that the uncleared material may undergo secondary necrosis with proinflammatory effects (1). These defects may have important effects in the lung, including perpetuating inflammation, infection, and tissue damage (3). A potential explanation for both the defective efferocytosis and subsequent chronic airway inflammation is the effect of microbial colonization of the airway. Bacterial colonization is commonly present in COPD, most frequently with Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis, and Pseudomonas aeruginosa, and has been shown to be independent of smoking status and associated with bronchial inflammation, increased exacerbations, and decline in FEV1 in COPD (4–7). Filamentous fungal colonization of the airways can also occur, although the clinical relevance is unclear. Isolation of fungi from sputum has been associated with reduced lung function in asthma and cystic fibrosis, although no such associations have been found in COPD (8). We hypothesized that the presence of potential pathogens in the airway could contribute to defective efferocytosis and associated airway inflammation in asymptomatic cigarette smokers and subjects with COPD.