RT Journal Article
SR Electronic
T1 Cigarette smoke and platelet-activating factor receptor dependent adhesion of <em>Streptococcus pneumoniae</em> to lower airway cells
JF Thorax
JO Thorax
FD BMJ Publishing Group Ltd and British Thoracic Society
SP 908
OP 913
DO 10.1136/thoraxjnl-2011-200835
VO 67
IS 10
A1 Jonathan Grigg
A1 Haydn Walters
A1 Sukhwinder Singh Sohal
A1 Richard Wood-Baker
A1 David W Reid
A1 Cang-Bao Xu
A1 Lars Edvinsson
A1 Mathieu C Morissette
A1 Martin R Stämpfli
A1 Michael Kirwan
A1 Lee Koh
A1 Reetika Suri
A1 Naseem Mushtaq
YR 2012
UL http://thorax.bmj.com/content/67/10/908.abstract
AB 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&lt;0.05 vs control), PAFR transcript level (p&lt;0.01), and PAFR expression (p&lt;0.01). Pneumococcal adhesion to A549 cells was attenuated by CV-3988 (p&lt;0.001). CSE 1% stimulated pneumococcal adhesion to BEAS2-B cells and HBEpC (p&lt;0.01 vs control). CSE 1% increased PAFR expression in BEAS2-B (p&lt;0.01), and in HBEpC (p&lt;0.05). Lung PAFR transcript level was increased in mice exposed to CS in vivo (p&lt;0.05 vs room air). Active smokers (n=16) had an increased percentage of bronchial epithelium with PAFR-positive cells (p&lt;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.