ArticleBiochemistry2006
CFTR Expression in human neutrophils and the phagolysosomal chlorination defect in cystic fibrosis.
Article in Biochemistry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 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
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Who cites it
151 citing papers in PubMed, 261 citations in OpenAlex.
- Altered Degranulation and pH of Neutrophil Phagosomes Impacts Antimicrobial Efficiency in Cystic Fibrosis.Frontiers in immunology · 2020Trial
- Galectin-9 signaling through TIM-3 is involved in neutrophil-mediated Gram-negative bacterial killing: an effect abrogated within the cystic fibrosis lung.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- Cystic fibrosis transmembrane conductance regulator recruitment to phagosomes in neutrophils.Journal of innate immunity · 2013Trial
- CFTR modulators exert subset-specific phenotype remodeling on circulating neutrophils in cystic fibrosis.ImmunoHorizons · 2026Article
- Considerations for early life genetic therapies in cystic fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2026Review
- Intrinsic neutrophil dysregulation in programmed cell death promotes neutrophilic inflammation in cystic fibrosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Article
- Myeloid cell-specific HMGB1 deficiency exaggerates mucoinflammatory responses but promotes bacterial clearance in mucoinflammatory lung disease.Scientific reports · 2026Article
- Microbial and host innate immune factors affecting the persistence ofFrontiers in cellular and infection microbiology · 2026Review
- The Challenges of Detecting Neutrophil CFTR.Journal of innate immunity · 2026Review
- Repurposing ivacaftor to attenuate LPS-induced acute lung injury: evidence from a non-cystic fibrosis model.Frontiers in pharmacology · 2026Article
- Article
- Neutrophil store-operated CaJournal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2025Article
- Neutrophils-astrocyte interactions in central nervous system inflammation.Cell death & disease · 2025Review
- CFTR negatively reprograms Th2 cell responses, and CFTR potentiation restrains allergic airway inflammation.JCI insight · 2025Article
- Inhibiting CFTR through inh-172 in primary neutrophils reveals CFTR-specific functional defects.Scientific reports · 2024Article
- E.PathDash, pathway activation analysis of publicly available pathogen gene expression data.mSystems · 2024Article
- A New Frontier in Cystic Fibrosis Pathophysiology: How and When Clock Genes Can Affect the Inflammatory/Immune Response in a Genetic Disease Model.Current issues in molecular biology · 2024Review
- Dysregulation of the Arachidonic Acid Pathway in Cystic Fibrosis: Implications for Chronic Inflammation and Disease Progression.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Analysis of CFTR mRNA and Protein in Peripheral Blood Mononuclear Cells via Quantitative Real-Time PCR and Western Blot.International journal of molecular sciences · 2024Article
- Pharmacological Improvement of Cystic Fibrosis Transmembrane Conductance Regulator Function Rescues Airway Epithelial Homeostasis and Host Defense in Children with Cystic Fibrosis.American journal of respiratory and critical care medicine · 2024Article
91 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Production of hypochlorous acid (HOCl) in neutrophils, a critical oxidant involved in bacterial killing, requires chloride anions. Because the primary defect of cystic fibrosis (CF) is the loss of chloride transport function of the CF transmembrane conductance regulator (CFTR), we hypothesized that CF neutrophils may be deficient in chlorination of bacterial components due to a limited chloride supply to the phagolysosomal compartment. Multiple approaches, including RT-PCR, immunofluorescence staining, and immunoblotting, were used to demonstrate that CFTR is expressed in resting neutrophils at the mRNA and protein levels. Probing fractions of resting neutrophils isolated by Percoll gradient fractionation and free flow electrophoresis for CFTR revealed its presence exclusively in secretory vesicles. The CFTR chloride channel was also detected in phagolysosomes, a special organelle formed after phagocytosis. Interestingly, HL-60 cells, a human promyelocytic leukemia cell line, upregulated CFTR expresssion when induced to differentiate into neutrophils with DMSO, strongly suggesting its potential role in mature neutrophil function. Analyses by gas chromatography and mass spectrometry (GC-MS) revealed that neutrophils from CF patients had a defect in their ability to chlorinate bacterial proteins from Pseudomonas aeruginosa metabolically prelabeled with [(13)C]-l-tyrosine, unveiling defective intraphagolysosomal HOCl production. In contrast, both normal and CF neutrophils exhibited normal extracellular production of HOCl when stimulated with phorbol ester, indicating that CF neutrophils had the normal ability to produce this oxidant in the extracellular medium. This report provides evidence which suggests that CFTR channel expression in neutrophils and its dysfunction affect neutrophil chlorination of phagocytosed bacteria.
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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.