ArticlePloS one2015
Pseudomonas aeruginosa Reduces VX-809 Stimulated F508del-CFTR Chloride Secretion by Airway Epithelial Cells.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Selection of reference genes for quantitative PCR: identifying reference genes for airway epithelial cells exposed toAmerican journal of physiology. Lung cellular and molecular physiology · 2020Pooled it
- Ivacaftor Reduces Inflammatory Mediators in Upper Airway Lining Fluid From Cystic Fibrosis Patients With a G551D Mutation: Serial Non-Invasive Home-Based Collection of Upper Airway Lining Fluid.Frontiers in immunology · 2021Trial
- Polymicrobial Extracellular Vesicles Reduce the Innate Immune Response of Human Cystic Fibrosis Bronchial Epithelial Cells.Journal of extracellular biology · 2026Article
- Outer membrane vesicles secreted byInfection and immunity · 2026Article
- Polymicrobial extracellular vesicles reduce the innate immune response of human cystic fibrosis bronchial epithelial cells.bioRxiv : the preprint server for biology · 2026Article
- Convergent strategies for nanobody-mediated inhibition of an epoxide hydrolase.bioRxiv : the preprint server for biology · 2026Article
- Evaluation of ATP12A and NFKBIZ as potential markers of inflammatory status in cystic fibrosis airway epithelial cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Let-7b-5p loaded Mesenchymal Stromal Cell Extracellular Vesicles reducebioRxiv : the preprint server for biology · 2025Article
- The potentiator ivacaftor is essential for pharmacological restoration of F508del-CFTR function and mucociliary clearance in cystic fibrosis.JCI insight · 2025Article
- Deleterious effect ofERJ open research · 2025Article
- Acute respiratory distress vs healthy lung environments differently affect mesenchymal stromal cell extracellular vesicle miRNAs.Cytotherapy · 2025Article
- Gene expression responses of CF airway epithelial cells exposed to elexacaftor/tezacaftor/ivacaftor suggest benefits beyond improved CFTR channel function.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Molecular basis for the transcriptional regulation of an epoxide-based virulence circuit in Pseudomonas aeruginosa.Nucleic acids research · 2024Article
- Molecular basis for the transcriptional regulation of an epoxide-based virulence circuit inbioRxiv : the preprint server for biology · 2024Article
- Article
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- Molecular and Functional Characteristics of Airway Epithelium under Chronic Hypoxia.International journal of molecular sciences · 2023Article
- Phenotypic Alteration of an Established Human Airway Cell Line by Media Selection.International journal of molecular sciences · 2023Article
- Modulator Combination Improves In Vitro the Microrheological Properties of the Airway Surface Liquid of Cystic Fibrosis Airway Epithelia.International journal of molecular sciences · 2022Article
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Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundP. aeruginosa is an opportunistic pathogen that chronically infects the lungs of 85% of adult patients with Cystic Fibrosis (CF). Previously, we demonstrated that P. aeruginosa reduced wt-CFTR Cl secretion by airway epithelial cells. Recently, a new investigational drug VX-809 has been shown to increase F508del-CFTR Cl secretion in human bronchial epithelial (HBE) cells, and, in combination with VX-770, to increase FEV1 (forced expiratory volume in 1 second) by an average of 3-5% in CF patients homozygous for the F508del-CFTR mutation. We propose that P. aeruginosa infection of CF lungs reduces VX-809 + VX-770- stimulated F508del-CFTR Cl secretion, and thereby reduces the clinical efficacy of VX-809 + VX-770. METHODS AND
resultsF508del-CFBE cells and primary cultures of CF-HBE cells (F508del/F508del) were exposed to VX-809 alone or a combination of VX-809 + VX-770 for 48 hours and the effect of P. aeruginosa on F508del-CFTR Cl secretion was measured in Ussing chambers. The effect of VX-809 on F508del-CFTR abundance was measured by cell surface biotinylation and western blot analysis. PAO1, PA14, PAK and 6 clinical isolates of P. aeruginosa (3 mucoid and 3 non-mucoid) significantly reduced drug stimulated F508del-CFTR Cl secretion, and plasma membrane F508del-CFTR.
conclusionThe observation that P. aeruginosa reduces VX-809 and VX-809 + VX-770 stimulated F508del CFTR Cl secretion may explain, in part, why VX-809 + VX-770 has modest efficacy in clinical trials.
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