Abstract
Pseudomonas aeruginosa is a major cause of pneumonia in patients with cystic fibrosis and other immuncompromising conditions. Here we showed that P. aeruginosa invades type I pneumocytes via a lipid raft-mediated mechanism. P. aeruginosa invasion of rat primary type I-like pneumocytes as well as a murine lung epithelial cell line 12 (MLE-12) is inhibited by drugs that remove membrane cholesterol and disrupt lipid rafts. Confocal microscopy demonstrated co-localization of intracellular P. aeruginosa with lipid raft components including caveolin-1 and -2. We generated caveolin-1 and -2 knockdowns in MLE-12 cells by using RNA interference techniques. Decreased expression of caveolin-2 significantly impaired the ability of P. aeruginosa to invade MLE-12 cells. In addition, the lipid raft-dependent tyrosine phosphorylation of caveolin-2 appeared to be a critical regulator of P. aeruginosa invasion.
Highlights
Monia in patients with cystic fibrosis and other im- cells have been implicated in a wide range of functions includmuncompromising conditions
P. aeruginosa Invades Type I Pneumocytes during the Pathogenesis of Pneumonia— P. aeruginosa frequently colonizes the upper airways of susceptible hosts, the development of P. aeruginosa pneumonia requires dissemination to the alveolar space prior to the development of epithelial cell damage and alveolar filling
We sought to determine whether P. aeruginosa invades type I pneumocytes during the pathogenesis of pneumonia by using a rat model of P. aeruginosa pneumonia
Summary
Monia in patients with cystic fibrosis and other im- cells have been implicated in a wide range of functions includmuncompromising conditions. We showed that P. aeruginosa invades type I pneumocytes via a lipid raft-mediated mechanism. P. aeruginosa invasion of rat primary type I-like pneumocytes as well as a murine lung epithelial cell line 12 (MLE-12) is inhibited by drugs that remove membrane cholesterol and disrupt lipid rafts. P. aeruginosa invasion of type I cells may facilitate dissemination throughout the host because of the single cell thickness of the alveolar epithelium. P. aeruginosa is able to invade nasal and bronchial epithelial cells via a lipid raft-dependent mechanism [13, 14]. An increasing number of pathogens have been recognized to co-opt the mechanism of lipid raft-mediated endocytosis in order to invade host cells [21,22,23,24]. P. aeruginosa may co-opt lipid raft-mediated endocytosis to invade the alveolar epithelium during the pathogenesis of P. aeruginosa pneumonia. The single cell thickness of the alveolar epithelium may lead to markedly different consequences for the host
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