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Cigarette smoke and platelet-activating factor receptor dependent adhesion of Streptococcus pneumoniae to lower airway cells

Grigg, Jonathan; Walters, Haydn; Sohal, Sukhwinder Singh; Wood-Baker, Richard; Reid, David W.; Xu, Cang-Bao LU ; Edvinsson, Lars LU ; Morissette, Mathieu C.; Staempfli, Martin R. and Kirwan, Michael, et al. (2012) In Thorax 67(10). p.908-913
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,... (More)
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. (Less)
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publication status
published
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in
Thorax
volume
67
issue
10
pages
908 - 913
publisher
BMJ Publishing Group
external identifiers
  • wos:000308708800014
  • scopus:84866083205
ISSN
1468-3296
DOI
10.1136/thoraxjnl-2011-200835
language
English
LU publication?
yes
id
8da27eb0-7cc1-492d-8ee7-20003ed51745 (old id 3135962)
date added to LUP
2012-11-01 16:16:45
date last changed
2017-09-24 03:59:22
@article{8da27eb0-7cc1-492d-8ee7-20003ed51745,
  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&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.},
  author       = {Grigg, Jonathan and Walters, Haydn and Sohal, Sukhwinder Singh and Wood-Baker, Richard and Reid, David W. and Xu, Cang-Bao and Edvinsson, Lars and Morissette, Mathieu C. and Staempfli, Martin R. and Kirwan, Michael and Koh, Lee and Suri, Reetika and Mushtaq, Naseem},
  issn         = {1468-3296},
  language     = {eng},
  number       = {10},
  pages        = {908--913},
  publisher    = {BMJ Publishing Group},
  series       = {Thorax},
  title        = {Cigarette smoke and platelet-activating factor receptor dependent adhesion of Streptococcus pneumoniae to lower airway cells},
  url          = {http://dx.doi.org/10.1136/thoraxjnl-2011-200835},
  volume       = {67},
  year         = {2012},
}