Cigarette smoke and platelet-activating factor receptor dependent adhesion of Streptococcus pneumoniae to lower airway cells. Issue 10 (1st May 2012)

• Record Type: Journal Article
• Authors: Grigg, Jonathan; Walters, Haydn; Sohal, Sukhwinder Singh; Wood-Baker, Richard; Reid, David W; Xu, Cang-Bao; Edvinsson, Lars; Morissette, Mathieu C; Stämpfli, Martin R; Kirwan, Michael; Koh, Lee; Suri, Reetika; Mushtaq, Naseem
• Is Part Of: Thorax. Volume 67:Issue 10(2012)
• Page Start: 908
• Page End: 913
• Publication Date: 2012-05-01
• Subjects: Cigarette smoke -- platelet-activating factor receptor -- Streptococcus pneumoniae -- adhesion -- airway epithelial cells -- asthma -- macrophage biology -- paediatric asthma -- paediatric lung disease -- paediatric physician -- asthma epidemiology -- asthma guidelines -- asthma mechanisms -- asthma pharmacology -- bronchoscopy -- COPD pathology -- COPD pharmacology -- airway epithelium -- COPD exacerbations -- emphysema -- cystic fibrosis -- innate immunity -- respiratory infection -- aspergillus lung disease -- assisted ventilation -- asthma genetics -- bacterial infection -- pneumonia; Chest -- Diseases -- Periodicals; Thorax; Chest -- Diseases; Periodicals; Periodicals; 617.54
• DOI: 10.1136/thoraxjnl-2011-200835
• Languages: English
• ISSNs: 0040-6376

Abstract

Abstract : Background: Exposure to cigarette smoke (CS) is associated with increased risk of pneumococcal infection. The mechanism for this association is unknown. We recently reported that the particulate matter from urban air simulates platelet-activating factor receptor (PAFR)-dependent adhesion of pneumococci to airway cells. We therefore sought to determine whether CS stimulates pneumococcal adhesion to airway cells. Methods: Human alveolar (A549), bronchial (BEAS2-B), and primary bronchial epithelial cells (HBEpC) were exposed to CS extract (CSE), and adhesion of Streptococcus pneumoniae determined. The role of PAFR in mediating adhesion was determined using a blocker (CV-3988). PAFR transcript level was assessed by quantitative real-time PCR, and PAFR expression by flow cytometry. Lung PAFR transcript level was assessed in mice exposed to CS, and bronchial epithelial PAFR expression assessed in active-smokers by immunostaining. Results: In A549 cells, CSE 1% increased pneumococcal adhesion (p<0.05 vs control), PAFR transcript level (p<0.01), and PAFR expression (p<0.01). Pneumococcal adhesion to A549 cells was attenuated by CV-3988 (p<0.001). CSE 1% stimulated pneumococcal adhesion to BEAS2-B cells and HBEpC (p<0.01 vs control). CSE 1% increased PAFR expression in BEAS2-B (p<0.01), and in HBEpC (p<0.05). Lung PAFR transcript level was increased in mice exposed to CS in vivo (p<0.05 vs room air). Active smokers (n=16) had an increased percentage of bronchial epithelium with PAFR-positive cells (p<0.05 vs never smokers, n=11). Conclusion: CSE stimulates PAFR-dependent pneumococcal adhesion to lower airway epithelial cells. We found evidence that CS increases bronchial PAFR in vivo.