ArticleProceedings of the National Academy of Sciences of the United States of America2008
Profound functional and signaling changes in viable inflammatory neutrophils homing to cystic fibrosis airways.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 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
89 citing papers in PubMed, 146 citations in OpenAlex.
- Trial
- 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
- Intrinsic neutrophil dysregulation in programmed cell death promotes neutrophilic inflammation in cystic fibrosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Article
- The Involvement of MicroRNAs in Innate Immunity and Cystic Fibrosis Lung Disease: A Narrative Review.Current issues in molecular biology · 2026Review
- Interkingdom signaling elicited by bacterial extracellular vesicles in human cystic fibrosis airway epithelium and neutrophils.Frontiers in cellular and infection microbiology · 2026Article
- Neutrophil Plasticity in Airway Disease: Balancing Damage and Repair.Journal of innate immunity · 2026Review
- Microbial and host innate immune factors affecting the persistence ofFrontiers in cellular and infection microbiology · 2026Review
- People with cystic fibrosis with high sputum neutrophil elastase on elexacaftor-tezacaftor-ivacaftor exhibit worse pulmonary function and pro-inflammatory airway milieu.Scientific reports · 2025Article
- Targeting CXCR2 signaling in inflammatory lung diseases: neutrophil-driven inflammation and emerging therapies.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Lung-kidney axis in cystic fibrosis: Early urinary markers of kidney injury correlate with neutrophil activation and worse lung function.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2025Article
- Innate Immunity in Cystic Fibrosis: Varied Effects of CFTR Modulator Therapy on Cell-to-Cell Communication.International journal of molecular sciences · 2025Review
- Review
- Epithelial extracellular vesicles induce inflammation and neutrophil activation in theFrontiers in immunology · 2025Article
- The heterogeneity of neutrophils in cancer and its implication for therapeutic targeting.Nature immunology · 2025Article
- Neutrophil extracellular traps are associated with airways inflammation and increased severity of lung disease in cystic fibrosis.ERJ open research · 2024Article
- Effects of hyperglycemia on airway epithelial barrier function in WT and CF 16HBE cells.Scientific reports · 2024Article
- Lung-Kidney Axis in Cystic Fibrosis: Early Urinary Markers of Kidney Injury Correlate with Neutrophil Activation and Worse Lung Function.medRxiv : the preprint server for health sciences · 2024Article
- Neutrophil-Derived Proteases in Lung Inflammation: Old Players and New Prospects.International journal of molecular sciences · 2024Review
- Aberrant immune programming in neutrophils in cystic fibrosis.Journal of leukocyte biology · 2024Article
- Sputum from People with Cystic Fibrosis Reduces the Killing of Methicillin-ResistantPathogens (Basel, Switzerland) · 2023Article
29 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
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Blood neutrophils recruited to cystic fibrosis (CF) airways are believed to be rapidly killed by resident bacteria and to passively release elastase and other toxic by-products that promote disease progression. By single-cell analysis, we demonstrate that profound functional and signaling changes readily occur within viable neutrophils recruited to CF airways, compared with their blood counterparts. Airway neutrophils have undergone conventional activation, as shown by decreased intracellular glutathione, increased lipid raft assembly, surface mobilization of CD11b+ and CD66b+ granules, and increased levels of the cytoskeleton-associated phospho-Syk kinase. Unexpectedly, they also mobilize to the surface CD63+ elastase-rich granules, usually confined intracellularly, and lose surface expression of CD16 and CD14, both key receptors in phagocytosis. Furthermore, they express CD80, major histocompatibility complex type II, and the prostaglandin D2 receptor CD294, all normally associated with other lineages, which reflects functional reprogramming. This notion is reinforced by their decreased total phosphotyrosine levels, mirroring a postactivated stage, and increased levels of the phospho-S6 ribosomal protein, a key anabolic switch. Thus, we identified a subset of neutrophils within CF airways with a viable but dysfunctional phenotype. This subset provides a possible therapeutic target and indicates a need to revisit current paradigms of CF airway disease.
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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.