ArticlePloS one2017
Regulation of xanthine dehydrogensase gene expression and uric acid production in human airway epithelial cells.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Long-term exposure to ambient air pollution and an increased risk of hyperuricemia.Clinical rheumatology · 2026Article
- A Multilevel Redox-Based Prognostic Model for Asthma Severity: From Genotype to Serum Biomarkers.Biomedicines · 2026Review
- Role of inflammasome in severe, steroid-resistant asthma.Current research in immunology · 2023Review
- Purine-Induced IFN-γ Promotes Uric Acid Production by Upregulating Xanthine Oxidoreductase Expression.Frontiers in immunology · 2022Article
- Potentiation of long-acting βRespiratory research · 2021Article
- Research Progress of Metabolomics in Asthma.Metabolites · 2021Review
- Modulation of cAMP metabolism for CFTR potentiation in human airway epithelial cells.Scientific reports · 2021Article
- Novel Pathway of Adenosine Generation in the Lungs from NADMolecules (Basel, Switzerland) · 2020Article
- Screen-Printed Glucose Sensors Modified with Cellulose Nanocrystals (CNCs) for Cell Culture Monitoring.Biosensors · 2020Article
- Inhibition of uric acid or IL-1β ameliorates respiratory syncytial virus immunopathology and development of asthma.Allergy · 2020Article
- Uric acid pathway activation during respiratory virus infection promotes Th2 immune response via innate cytokine production and ILC2 accumulation.Mucosal immunology · 2020Article
- ABCF1 Regulates dsDNA-induced Immune Responses in Human Airway Epithelial Cells.Frontiers in cellular and infection microbiology · 2020Article
- The different faces of the macrophage in asthma.Current opinion in pulmonary medicine · 2020Review
- The impact of cigarette smoke exposure, COPD, or asthma status on ABC transporter gene expression in human airway epithelial cells.Scientific reports · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe airway epithelium is a physical and immunological barrier that protects the pulmonary system from inhaled environmental insults. Uric acid has been detected in the respiratory tract and can function as an antioxidant or damage associated molecular pattern. We have demonstrated that human airway epithelial cells are a source of uric acid. Our hypothesis is that uric acid production by airway epithelial cells is induced by environmental stimuli associated with chronic respiratory diseases. We therefore examined how airway epithelial cells regulate uric acid production. MATERIALS AND
methodsAllergen and cigarette smoke mouse models were performed using house dust mite (HDM) and cigarette smoke exposure, respectively, with outcome measurements of lung uric acid levels. Primary human airway epithelial cells isolated from clinically diagnosed patients with asthma and chronic obstructive pulmonary disease (COPD) were grown in submerged cultures and compared to age-matched healthy controls for uric acid release. HBEC-6KT cells, a human airway epithelial cell line, were grown under submerged monolayer conditions for mechanistic and gene expression studies.
resultsHDM, but not cigarette smoke exposure, stimulated uric acid production in vivo and in vitro. Primary human airway epithelial cells from asthma, but not COPD patients, displayed elevated levels of extracellular uric acid in culture. In HBEC-6KT, production of uric acid was sensitive to the xanthine dehydrogenase (XDH) inhibitor, allopurinol, and the ATP Binding Cassette C4 (ABCC4) inhibitor, MK-571. Lastly, the pro-inflammatory cytokine combination of TNF-α and IFN-γ elevated extracellular uric acid levels and XDH gene expression in HBEC-6KT cells.
conclusionsOur results suggest that the active production of uric acid from human airway epithelial cells may be intrinsically altered in asthma and be further induced by pro-inflammatory cytokines.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.