ArticleScientific reports2020
Altered iron metabolism in cystic fibrosis macrophages: the impact of CFTR modulators and implications for Pseudomonas aeruginosa survival.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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.
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
28 citing papers in PubMed, 35 citations in OpenAlex.
- The response regulator BqsR/CarR controls FeNature communications · 2026Article
- Article
- Phage-Based Approaches to ChronicAntibiotics (Basel, Switzerland) · 2026Review
- The response regulator BqsR/CarR controls ferrous iron (FebioRxiv : the preprint server for biology · 2025Article
- Article
- ThebioRxiv : the preprint server for biology · 2025Article
- The impact of cystic fibrosis transmembrane conductance regulator (CFTR) modulators on the pulmonary microbiota.Microbiology (Reading, England) · 2025Review
- Iron Supplementation in Anemic Patients with Cystic Fibrosis: Effects on Hematologic, Clinical, and Pulmonary Outcomes.Tanaffos · 2025Article
- Wound repair and immune function in theFrontiers in cellular and infection microbiology · 2025Review
- 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
- Real-world impact of ivacaftor in people with cystic fibrosis and select ivacaftor-responsive mutations.BMJ open respiratory research · 2024Observational
- CFTR is required for zinc-mediated antibacterial defense in human macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Oxidative Stress Biomarkers in Cystic Fibrosis and Cystic Fibrosis-Related Diabetes in Children: A Literature Review.Biomedicines · 2023Review
- Comparative effects of CFTR modulators on phagocytic, metabolic and inflammatory profiles of CF and nonCF macrophages.Scientific reports · 2023Article
- Cystic fibrosis macrophage function and clinical outcomes after elexacaftor/tezacaftor/ivacaftor.The European respiratory journal · 2023Article
- Revisiting Host-Pathogen Interactions in Cystic Fibrosis Lungs in the Era of CFTR Modulators.International journal of molecular sciences · 2023Review
- Single-Cell RNA Sequencing Reveals New Basic and Translational Insights in the Cystic Fibrosis Lung.American journal of respiratory cell and molecular biology · 2023Review
- Loss of CFTR function in macrophages alters the cell transcriptional program and delays lung resolution of inflammation.Frontiers in immunology · 2023Article
- ScRNA-seq expression ofLife science alliance · 2022Article
- Impact ofInternational journal of molecular sciences · 2022Review
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 1 country.
Funding
Abstract
Cystic fibrosis (CF) is a genetic disease caused by mutations in the CF transmembrane conductance regulator (CFTR) gene, resulting in chronic bacterial lung infections and tissue damage. CF macrophages exhibit reduced bacterial killing and increased inflammatory signaling. Iron is elevated in the CF lung and is a critical nutrient for bacteria, including the common CF pathogen Pseudomonas aeruginosa (Pa). While macrophages are a key regulatory component of extracellular iron, iron metabolism has yet to be characterized in human CF macrophages. Secreted and total protein levels were analyzed in non-CF and F508del/F508del CF monocyte derived macrophages (MDMs) with and without clinically approved CFTR modulators ivacaftor/lumacaftor. CF macrophage transferrin receptor 1 (TfR1) was reduced with ivacaftor/lumacaftor treatment. When activated with LPS, CF macrophage expressed reduced ferroportin (Fpn). After the addition of exogenous iron, total iron was elevated in conditioned media from CF MDMs and reduced in conditioned media from ivacaftor/lumacaftor treated CF MDMs. Pa biofilm formation and viability were elevated in conditioned media from CF MDMs and biofilm formation was reduced in the presence of conditioned media from ivacaftor/lumacaftor treated CF MDMs. Defects in iron metabolism observed in this study may inform host-pathogen interactions between CF macrophages and Pa.
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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.