Enhanced platelet activating factor receptor (PAFR) expression in smoker airways

Introduction: Cigarette smoking increases the risk of pneumococcal disease, and epidemiologic studies suggest that air pollution from cigarette smoke increases vulnerability to bacterial pneumonia. We have shown that inhalable particulate matter (PM) stimulates pneumococcal adhesion to human lower airway cells. Increased pneumococcal adhesion is associated with increased invasiveness of bacteria. Oxidative stress mediates the adhesive response of airway epithelial cells, and platelet activating factor receptor (PAFR) is a receptor co-opted by pneumococci to facilitate PM-stimulated adhesion. Objective: To investigate the expression of PAFR in the airways of normal lung function smokers (NS) in vivo. Methods: Endobronchial biopsies from 16 NS and 11 normal controls (NC) were stained for anti-PAFR monoclonal antibody. PAFR expression was assessed as percentage of epithelium stained for PAFR over total basement membrane length by using computer-assisted image analysis. Results: Percentage of epithelial staining for PAFR was increased significantly in NS (A) compared to NC (B) (Chi-Square=30.3, 0 (0–4.8), p<0.001). Conclusions: This is the first description of in-vivo expression of PAFR in the epithelium of NS compared to NC. Our data suggest that enhanced PAFR expression may be the mechanism of increased vulnerability of smokers to pneumococcal infection.