Pseudomonas Invasion of Type I Pneumocytes Is Dependent on the Expression and Phosphorylation of Caveolin-2

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 m...

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Veröffentlicht in:The Journal of biological chemistry 2005-02, Vol.280 (6), p.4864-4872
Hauptverfasser: Zaas, David W., Duncan, Mathew J., Li, Guojie, Wright, Jo Rae, Abraham, Soman N.
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Sprache:eng
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Zusammenfassung: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.
ISSN:0021-9258
1083-351X
DOI:10.1074/jbc.M411702200