ArticleThorax2018
Delayed neutrophil apoptosis enhances NET formation in cystic fibrosis.
Article in Thorax, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07692594 (Cardiovascular Health in People With Cystic Fibrosis), which is not on this map. Cited by 129 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.
Cardiovascular Health in People With Cystic Fibrosis
Who cites it
129 citing papers in PubMed, 197 citations in OpenAlex.
- CFTR modulators exert subset-specific phenotype remodeling on circulating neutrophils in cystic fibrosis.ImmunoHorizons · 2026Article
- Cystic fibrosis: insights from zebrafish models.Disease models & mechanisms · 2026Review
- Cell death crosstalk in NET-Driven inflammation: mechanisms, disease contexts, and therapeutic perspectives.Biomarker research · 2026Review
- Intrinsic neutrophil dysregulation in programmed cell death promotes neutrophilic inflammation in cystic fibrosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Article
- Simplified flow cytometric quantification of human neutrophil extracellular traps (NETs).Journal of inflammation (London, England) · 2026Article
- Article
- Modulation of immune responses by elexacaftor/tezacaftor/ivacaftor therapy in cystic fibrosis: data from a compassionate use program.Respiratory research · 2026Article
- The Involvement of MicroRNAs in Innate Immunity and Cystic Fibrosis Lung Disease: A Narrative Review.Current issues in molecular biology · 2026Review
- Neutrophil extracellular traps and acute kidney injury: a narrative review.Frontiers in immunology · 2026Review
- Microbial and host innate immune factors affecting the persistence ofFrontiers in cellular and infection microbiology · 2026Review
- Injectable cationic dynamic hydrogel with supramolecular drug loading reprograms neutrophil fate to alleviate diabetic periodontitis.Materials today. Bio · 2025Article
- Transcriptomic and functional responses of the cystic fibrosis airway epithelium to CFTR modulator therapy.JCI insight · 2025Article
- Advanced Nanoparticle Therapeutics for Targeting Neutrophils in Inflammatory Diseases.Advanced healthcare materials · 2025Review
- Neutrophil death-more than meets the eye.Experimental hematology · 2025Review
- Apoptotic bodies derived from hypoxic bone marrow mesenchymal stem cells reverse LPS-induced apoptosis delay in neutrophils.Stem cells translational medicine · 2025Article
- Dual Nature of Neutrophil Extracellular Traps (NETs)-From Cancer's Ally to Therapeutic Target.Cells · 2025Review
- Drug repurposing of cyclin-dependent kinase inhibitors for neutrophilic acute respiratory distress syndrome and psoriasis.Journal of advanced research · 2025Review
- A Bifunctional Antibody Targeting PD-1 and TGF-β Signaling Has Antitumor Activity in Combination with Radiotherapy and Attenuates Radiation-Induced Lung Injury.Cancer immunology research · 2025Article
- Managing an ageing cystic fibrosis population: challenges and priorities.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Chronic Coinfection with Pseudomonas aeruginosa and Normal Colony Staphylococcus aureus Causes Lung Structural Damage in the Cystic Fibrosis Rat.The American journal of pathology · 2025Article
69 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
22 authors at 5 institutions in 3 countries.
Funding
Abstract
backgroundCystic fibrosis (CF) lung disease is defined by large numbers of neutrophils and associated damaging products in the airway. Delayed neutrophil apoptosis is described in CF although it is unclear whether this is a primary neutrophil defect or a response to chronic inflammation. Increased levels of neutrophil extracellular traps (NETs) have been measured in CF and we aimed to investigate the causal relationship between these phenomena and their potential to serve as a driver of inflammation. We hypothesised that the delay in apoptosis in CF is a primary defect and preferentially allows CF neutrophils to form NETs, contributing to inflammation.
methodsBlood neutrophils were isolated from patients with CF, CF pigs and appropriate controls. Neutrophils were also obtained from patients with CF before and after commencing ivacaftor. Apoptosis was assessed by morphology and flow cytometry. NET formation was determined by fluorescent microscopy and DNA release assays. NET interaction with macrophages was examined by measuring cytokine generation with ELISA and qRT-PCR.
resultsCF neutrophils live longer due to decreased apoptosis. This was observed in both cystic fibrosis transmembrane conductance regulator (CFTR) null piglets and patients with CF, and furthermore was reversed by ivacaftor (CFTR potentiator) in patients with gating (G551D) mutations. CF neutrophils formed more NETs and this was reversed by cyclin-dependent kinase inhibitor exposure. NETs provided a proinflammatory stimulus to macrophages, which was enhanced in CF.
conclusionsCF neutrophils have a prosurvival phenotype that is associated with an absence of CFTR function and allows increased NET production, which can in turn induce inflammation. Augmenting neutrophil apoptosis in CF may allow more appropriate neutrophil disposal, decreasing NET formation and thus inflammation.
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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.