ArticlePloS one2012
Lipoxin A4 stimulates calcium-activated chloride currents and increases airway surface liquid height in normal and cystic fibrosis airway epithelia.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 51 citations in OpenAlex.
- Lipoxins as Modulators of Diseases.Cells · 2025Review
- Specialized Pro-Resolving Lipid Mediators in Pulmonary Diseases: Molecular and Therapeutic Implications.Molecules (Basel, Switzerland) · 2025Review
- Specialized proresolving mediator resolvin E1 corrects the altered cystic fibrosis nasal epithelium cilia beating dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Intercellular Communication in Airway Epithelial Cell Regeneration: Potential Roles of Connexins and Pannexins.International journal of molecular sciences · 2023Review
- The Impact of Air Pollution on the Course of Cystic Fibrosis: A Review.Frontiers in physiology · 2022Review
- Hyperinflammation and airway surface liquid dehydration in cystic fibrosis: purinergic system as therapeutic target.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Review
- Resolution-Based Therapies: The Potential of Lipoxins to Treat Human Diseases.Frontiers in immunology · 2021Review
- The Resolution Approach to Cystic Fibrosis Inflammation.Frontiers in pharmacology · 2020Review
- The Role of Specialized Pro-Resolving Mediators in Cystic Fibrosis Airways Disease.Frontiers in pharmacology · 2020Review
- Review
- Airway surface liquid acidification initiates host defense abnormalities in Cystic Fibrosis.Scientific reports · 2019Article
- Roles, Actions, and Therapeutic Potential of Specialized Pro-resolving Lipid Mediators for the Treatment of Inflammation in Cystic Fibrosis.Frontiers in pharmacology · 2019Review
- Specialized Pro-Resolving Lipid Mediators in Cystic Fibrosis.International journal of molecular sciences · 2018Review
- Specialized Proresolving Mediators in Innate and Adaptive Immune Responses in Airway Diseases.Physiological reviews · 2018Review
- microRNA-181b is increased in cystic fibrosis cells and impairs lipoxin AScientific reports · 2017Article
- Pro-resolving lipid mediator Resolvin D1 serves as a marker of lung disease in cystic fibrosis.PloS one · 2017Article
- Review
- Article
- Control of local immunity by airway epithelial cells.Mucosal immunology · 2016Review
- Modulation of the Activities of Neuronal Ion Channels by Fatty Acid-Derived Pro-Resolvents.Frontiers in physiology · 2016Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cystic Fibrosis (CF) is a genetic disease characterised by a deficit in epithelial Cl(-) secretion which in the lung leads to airway dehydration and a reduced Airway Surface Liquid (ASL) height. The endogenous lipoxin LXA(4) is a member of the newly identified eicosanoids playing a key role in ending the inflammatory process. Levels of LXA(4) are reported to be decreased in the airways of patients with CF. We have previously shown that in normal human bronchial epithelial cells, LXA(4) produced a rapid and transient increase in intracellular Ca(2+). We have investigated, the effect of LXA(4) on Cl(-) secretion and the functional consequences on ASL generation in bronchial epithelial cells obtained from CF and non-CF patient biopsies and in bronchial epithelial cell lines. We found that LXA(4) stimulated a rapid intracellular Ca(2+) increase in all of the different CF bronchial epithelial cells tested. In non-CF and CF bronchial epithelia, LXA(4) stimulated whole-cell Cl(-) currents which were inhibited by NPPB (calcium-activated Cl(-) channel inhibitor), BAPTA-AM (chelator of intracellular Ca(2+)) but not by CFTRinh-172 (CFTR inhibitor). We found, using confocal imaging, that LXA(4) increased the ASL height in non-CF and in CF airway bronchial epithelia. The LXA(4) effect on ASL height was sensitive to bumetanide, an inhibitor of transepithelial Cl(-) secretion. The LXA(4) stimulation of intracellular Ca(2+), whole-cell Cl(-) currents, conductances and ASL height were inhibited by Boc-2, a specific antagonist of the ALX/FPR2 receptor. Our results provide, for the first time, evidence for a novel role of LXA(4) in the stimulation of intracellular Ca(2+) signalling leading to Ca(2+)-activated Cl(-) secretion and enhanced ASL height in non-CF and CF bronchial epithelia.
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