Fluticasone propionate reduces bacterial airway epithelial invasion

Fluticasone propionate reduces the frequency and severity of the episodes of exacerbation of chronic obstructive pulmonary disease (COPD). Streptococcus pneumoniae and Haemophilus influenzae are frequently isolated in these episodes. Both express phosphorylcholine, an epitope that mediates their interaction with airway epithelial cells via the platelet-activating factor receptor (PAFR). The present work studies the effects of fluticasone propionate on the expression of PAFR on human airway epithelial cells, the invasion of these cells by S. pneumoniae and H. influenzae, and the course of pneumococcal infection in vivo. The following were used in the experiments: S. pneumoniae and H. influenzae isolated from patients with COPD, cell cultures of type II pneumocytes and bronchoepithelial cells, and a mouse model of lung infection. Fluticasone propionate was found to reduce PAFR expression on the surface of the two cells types studied. All S. pneumoniae and H. influenzae isolates expressed phosphorylcholine. Treatment of both cells lines with fluticasone propionate reduced invasion of both microorganisms and reduced the bacterial load of mice infected with S. pneumoniae. Fluticasone propionate reduces the invasion of airway epithelial cells by Streptococcus pneumoniae and Haemophilus influenzae through its effect on platelet-activating factor receptor. These results may help explain the beneficial effects of fluticasone propionate on chronic obstructive pulmonary disease exacerbations.