Fluticasone propionate reduces bacterial airway epithelial invasion

¹ Institut Universitari dInvestigacions en Ciències de la Salut (IUNICS), Universitat de les Illes Balears (UIB), Palma de Mallorca, Spain
² Servicio de Neumología, Hospital Son Dureta, Fundación Caubet-Cimera and CIBER Enfermedades Respiratorias, Palma de Mallorca, Spain

^* To whom correspondence should be addressed. E-mail: sebastian.alberti{at}uib.es.

	Abstract

Fluticasone propionate (FP) 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, a epitope that mediates their interaction with airway epithelial cells via the platelet-activating factor receptor (PAFR).

We studied the effects of FP 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.

For experiments, we used S. pneumoniae and H. influenzae isolated from patients with COPD, cell cultures of type II pneumocytes and bronchoepithelial cells, and a mice model of lung infection.

We found that: FP reduced the expression of PAFR on the surface of two types of cells studied; All S. pneumoniae and H. influenzae isolates expressed phosphorylcholine; Treatment of both cells lines with FP reduced invasion of both microorganisms; and, FP reduced the bacterial load of mice infected with S. pneumoniae.

FP reduces the invasion of airway epithelial cells by S. pneumoniae and H. influenzae through its effect on PAFR. These results may contribute to explain the beneficial effects of FP on COPD exacerbations.