ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012
Does the F508-CFTR mutation induce a proinflammatory response in human airway epithelial cells?
Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
What it found
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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
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 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
- Functional CFTR may be required for Prevotella melaninogenica regulation of epithelial cell defense against Staphylococcus aureus.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2026Article
- Recent developments in cystic fibrosis drug discovery: where are we today?Expert opinion on drug discovery · 2025Review
- Epidemiological Profile of Hospitalized Patients with Cystic Fibrosis in Brazil Due to Severe Acute Respiratory Infection during the COVID-19 Pandemic and a Systematic Review of Worldwide COVID-19 in Those with Cystic Fibrosis.Healthcare (Basel, Switzerland) · 2023Article
- Current concepts on Pseudomonas aeruginosa interaction with human airway epithelium.PLoS pathogens · 2023Review
- Mutation-class dependent signatures outweigh disease-associated processes in cystic fibrosis cells.Cell & bioscience · 2023Article
- A novel in vitro model to study prolonged Pseudomonas aeruginosa infection in the cystic fibrosis bronchial epithelium.PloS one · 2023Article
- SARS-CoV-2 Infection in Patients with Cystic Fibrosis: What We Know So Far.Life (Basel, Switzerland) · 2022Review
- Bronchial epithelial DNA methyltransferase 3b dampens pulmonary immune responses during Pseudomonas aeruginosa infection.PLoS pathogens · 2021Article
- Case Report: Analysis of Inflammatory Cytokines IL-6, CCL2/MCP1, CCL5/RANTES, CXCL9/MIG, and CXCL10/IP10 in a Cystic Fibrosis Patient Cohort During the First Wave of the COVID-19 Pandemic.Frontiers in pediatrics · 2021Article
- Myeloid CFTR loss-of-function causes persistent neutrophilic inflammation in cystic fibrosis.Journal of leukocyte biology · 2020Article
- SARS-CoV-2 (COVID-19) and cystic fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- CK19 stabilizes CFTR at the cell surface by limiting its endocytic pathway degradation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Transcriptional consequences of impaired immune cell responses induced by cystic fibrosis plasma characterized via dual RNA sequencing.BMC medical genomics · 2019Article
- Transcriptome Profiling and Molecular Therapeutic Advances in Cystic Fibrosis: Recent Insights.Genes · 2019Review
- Cystic Fibrosis Airway Microbiome: Overturning the Old, Opening the Way for the New.Journal of bacteriology · 2018Review
- Connectivity mapping (ssCMap) to predict A20-inducing drugs and their antiinflammatory action in cystic fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Chemotaxis and Binding of Pseudomonas aeruginosa to Scratch-Wounded Human Cystic Fibrosis Airway Epithelial Cells.PloS one · 2016Article
- CFTR Controls the Activity of NF-κB by Enhancing the Degradation of TRADD.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2016Article
- Salt, chloride, bleach, and innate host defense.Journal of leukocyte biology · 2015Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
In the clinical setting, mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene enhance the inflammatory response in the lung to Pseudomonas aeruginosa (P. aeruginosa) infection. However, studies on human airway epithelial cells in vitro have produced conflicting results regarding the effect of mutations in CFTR on the inflammatory response to P. aeruginosa, and there are no comprehensive studies evaluating the effect of P. aeruginosa on the inflammatory response in airway epithelial cells with the ΔF508/ΔF508 genotype and their matched CF cell line rescued with wild-type (wt)-CFTR. CFBE41o- cells (ΔF508/ΔF508) and CFBE41o- cells complemented with wt-CFTR (CFBE-wt-CFTR) have been used extensively as an experimental model to study CF. Thus the goal of this study was to examine the effect of P. aeruginosa on gene expression and cytokine/chemokine production in this pair of cells. P. aeruginosa elicited a more robust increase in cytokine and chemokine expression (e.g., IL-8, CXCL1, CXCL2 and TNF-α) in CFBE-wt-CFTR cells compared with CFBE-ΔF508-CFTR cells. These results demonstrate that CFBE41o- cells complemented with wt-CFTR mount a more robust inflammatory response to P. aeruginosa than CFBE41o-ΔF508/ΔF508-CFTR cells. Taken together with other published studies, our data demonstrate that there is no compelling evidence to support the view that mutations in CFTR induce a hyperinflammatory response in human airway epithelial cells in vivo. Although the lungs of patients with CF have abundant levels of proinflammatory cytokines and chemokines, because the lung is populated by immune cells and epithelial cells there is no way to know, a priori, whether airway epithelial cells in the CF lung in vivo are hyperinflammatory in response to P. aeruginosa compared with non-CF lung epithelial cells. Thus studies on human airway epithelial cell lines and primary cells in vitro that propose to examine the effect of mutations in CFTR on the inflammatory response to P. aeruginosa have uncertain clinical significance with regard to CF.
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Registered trials
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