ArticleBMC immunology2021
Neutrophil extracellular traps are present in the airways of ENaC-overexpressing mice with cystic fibrosis-like lung disease.
Article in BMC immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 26 citations in OpenAlex.
- Myeloperoxidase and Other Markers of Neutrophil Activation Associate With Malaria and Malaria/HIV Coinfection in the Human Placenta.Frontiers in immunology · 2021Trial
- SARS-CoV-2 infection produces an IL-33-dependent chronic eosinophilic pneumonia and muco-inflammatory airways disease in Scnn1b-Tg mice.JCI insight · 2026Article
- Spectral Flow Cytometry Method for Immunophenotyping Neutrophil Activation and NETs in an Acute Dust Exposure Model.Immunity, inflammation and disease · 2026Article
- Microenvironmental effects of a non-antibiotic therapy for a chronic Polymicrobial infection Alter microbial physiology, competition, and virulence.The ISME journal · 2026Article
- Immunogenicity and plasmid delivery pathways of non-invasiveInfection and immunity · 2026Article
- Inflammation and epithelial-mesenchymal transition in a CFTR-depleted human bronchial epithelial cell line revealed by proteomics and human organ-on-a-chip.The FEBS journal · 2025Article
- The bacterial serine protease inhibitor ecotin inhibits neutrophil elastase enzymatic activity in cystic fibrosis sputa.Heliyon · 2024Article
- Flagellum-deficientMicrobiology spectrum · 2024Article
- Chronic hyperglycemia aggravates lung function in aAmerican journal of physiology. Lung cellular and molecular physiology · 2024Article
- Aberrant immune programming in neutrophils in cystic fibrosis.Journal of leukocyte biology · 2024Article
- Article
- Biologically Relevant Murine Models of ChronicPathogens (Basel, Switzerland) · 2023Article
- Neutrophil Extracellular Traps in Airway Diseases: Pathological Roles and Therapeutic Implications.International journal of molecular sciences · 2023Review
- Airway mucus in pulmonary diseases: Muco-adhesive and muco-penetrating particles to overcome the airway mucus barriers.International journal of pharmaceutics · 2023Review
- Inhibition of Myeloperoxidase Pro-Fibrotic Effect by Noscapine in Equine Endometrium.International journal of molecular sciences · 2023Article
- Role of epithelial sodium channel-related inflammation in human diseases.Frontiers in immunology · 2023Review
- Oral administration ofBioscience of microbiota, food and health · 2023Article
- Dual oxidase 1 is dispensable duringFrontiers in immunology · 2023Article
- The changing landscape of the cystic fibrosis lung environment: From the perspective of Pseudomonas aeruginosa.Current opinion in pharmacology · 2022Review
- Spotlighting "Neutrophil Elastase Triggers the Release of Macrophage Extracellular Traps": A New Catch in Cystic Fibrosis?American journal of respiratory cell and molecular biology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundNeutrophils are key components of the exacerbated inflammation and tissue damage in cystic fibrosis (CF) airways. Neutrophil extracellular traps (NETs) trap and kill extracellular pathogens. While NETs are abundant in the airways of CF patients and have been hypothesized to contribute to lung damage in CF, the in vivo role of NETs remains controversial, partially due to lack of appropriate animal models. The goal of this study was to detect NETs and to further characterize neutrophil-mediated inflammation in the airways of mice overexpressing the epithelial sodium channel (βENaC-Tg mice on C57BL/6 background) in their lung with CF-like airway disease, in the absence of any apparent bacterial infections.
methodsHistology scoring of lung tissues, flow cytometry, multiplex ELISA, immunohistochemistry and immunofluorescence were used to characterize NETs and the airway environment in uninfected, βENaC-Tg mice at 6 and 8 weeks of age, the most chronic time points so far studied in this model.
resultsExcessive neutrophilic infiltration characterized the lungs of uninfected, βENaC-Tg mice at 6 and 8 weeks of age. The bronchoalveolar lavage fluid (BALF) of βENaC-Tg mice contains increased levels of CF-associated cytokines and chemokines: KC, MIP-1α/β, MCP-1, G-CSF, IL-5, and IL-6. The BALF of βENaC-Tg mice contain MPO-DNA complexes, indicative of the presence of NETs. Immunofluorescence and flow cytometry of BALF neutrophils and lung tissues demonstrated increased histone citrullination, a NET-specific marker, in βENaC-Tg mice.
conclusionsNETs are detected in the airways of βENaC-Tg mice, in the absence of bacterial infections. These data demonstrate the usefulness of the βENaC-Tg mouse to serve as a model for studying the role of NETs in chronic CF airway inflammation.
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.