2006
DOI: 10.1152/ajpcell.00108.2005
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Pseudomonas aeruginosainhibits endocytic recycling of CFTR in polarized human airway epithelial cells

Abstract: The most common mutation in the CFTR gene in individuals with cystic fibrosis (CF), DeltaF508, leads to the absence of CFTR Cl(-) channels in the apical plasma membrane, which in turn results in impairment of mucociliary clearance, the first line of defense against inhaled bacteria. Pseudomonas aeruginosa is particularly successful at colonizing and chronically infecting the lungs and is responsible for the majority of morbidity and mortality in patients with CF. Rescue of DeltaF508-CFTR by reduced temperature… Show more

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Cited by 65 publications
(91 citation statements)
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References 71 publications
(75 reference statements)
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“…Previous studies have demonstrated that mature, glycosylated ⌬F508-CFTR is expressed at the apical plasma membrane both in parental CFBE41o-cells and in CFBEϩ⌬F508 cells at 37°C, and shown that significant amounts of ⌬F508-CFTR are rescued by incubation at 27°C in the transduced cell line (30,35). Other studies have shown that the CFBEϩ⌬F508 cells express functional ⌬F508-CFTR chloride channels (34).…”
Section: Resultsmentioning
confidence: 99%
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“…Previous studies have demonstrated that mature, glycosylated ⌬F508-CFTR is expressed at the apical plasma membrane both in parental CFBE41o-cells and in CFBEϩ⌬F508 cells at 37°C, and shown that significant amounts of ⌬F508-CFTR are rescued by incubation at 27°C in the transduced cell line (30,35). Other studies have shown that the CFBEϩ⌬F508 cells express functional ⌬F508-CFTR chloride channels (34).…”
Section: Resultsmentioning
confidence: 99%
“…Electrophysiology-Seven days after seeding monolayers, Ussing chamber measurements were performed essentially as described (34), except that 50 M amiloride was used. For these studies, 50 M genistein was applied apically to activate temperature-rescued ⌬F508-CFTR channels (34,35).…”
Section: Methodsmentioning
confidence: 99%
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“…Once chronic infection is established, P. aeruginosa is virtually impossible to eradicate and is associated with increased mortality and morbidity in CF patients. 10 Investigations of the nosocomial epidemiology of P. aeruginosa have been hampered by the inadequate discriminatory ability of classical phenotypic methods such as serotyping, phage and pyocin typing, and biotyping. 11,12 Modern DNA-based techniques, such as enterobacterial repetitive intergenic consensus PCR (ERIC-PCR) and Ribotyping, have been widely used in the epidemiological investigation of many microorganisms, including P. aeruginosa.…”
Section: Introductionmentioning
confidence: 99%
“…Among these is the CFTR inhibitory factor (Cif), a recently characterized P. aeruginosa protein expressed both in the PA14 strain and in clinical isolates (20,21). Originally characterized as an extracellular factor that inhibited CFTR-mediated chloride currents across polarized epithelial monolayers (22), Cif is both directly secreted and is also packaged into outer membrane vesicles that dramatically enhance delivery to airway epithelial cells (23). Further investigation revealed that Cif acts by triggering the post-endocytic degradation of CFTR, reducing its cell-surface abundance (22).…”
mentioning
confidence: 99%