Abstract
Background: Although the mechanism is unknown, cigarette smoke exposure increases the risk of pneumococcal infections in humans1. We have recently shown that fossil fuel derived particulate matter increases adhesion of S. pneumoniae via upregulation of platelet activating factor receptor (PAFr) expression on airway cells2. We therefore aimed to assess whether cigarette smoke extract (CSE) upregulates the PAFr expression in vitro.
Methods: The human lung epithelial (A549) cell line was incubated with very low concentrations of CSE (0.01%, 0.02% and 0.05%) for 4 hr. PAFr expression, adjusted for non-specific staining, was then assessed by flow cytometry using a PAFr human monoclonal antibody.
Results: CSE stimulated dose-dependent increase in PAFr expression, with an increase in mean PAFr fluorescence and % positivity (Figure 1 and Table 1).
Conclusion: CSE stimulates PAFr, the receptor for S. pneumoniae adhesion to lower airway cells, and may be the mechanisms underlying the epidemiological association between active and passive cigarette exposure and invasive pneumococcal disease in adults and children.
FACs analysis showing a dose response relationship between CSE and PAFr expression.
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