ArticleImmunoHorizons2022
Fibrotic Lung Disease Alters Neutrophil Trafficking and Promotes Neutrophil Elastase and Extracellular Trap Release.
Article in ImmunoHorizons, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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Who cites it
21 citing papers in PubMed, 22 citations in OpenAlex.
- Convergent Microenvironment Linking Idiopathic Pulmonary Fibrosis and Lung Cancer.Expert reviews in molecular medicine · 2026Review
- Repeated air pollution exposure predisposes to adverse outcomes from acute lung injury.Particle and fibre toxicology · 2026Article
- Spectral Flow Cytometry Method for Immunophenotyping Neutrophil Activation and NETs in an Acute Dust Exposure Model.Immunity, inflammation and disease · 2026Article
- Neutrophil extracellular traps in pulmonary fibrosis: mechanisms, immunity and therapeutic targets.Frontiers in immunology · 2026Review
- Modulatory roles of the vagus nerve and nicotine in bleomycin-induced pulmonary fibrosis in rats.BMC pulmonary medicine · 2025Article
- Variable steady inflammation and inflammatory responses in precision-cut lung slices from various IPF lung Regions.Respiratory research · 2025Article
- Neutrophils in idiopathic pulmonary fibrosis patients are phenotypically distinct from controls.ERJ open research · 2025Article
- A Simple Ratio in a Complex Disease: Exploring the Neutrophil-to-Lymphocyte Ratio in Idiopathic Pulmonary Fibrosis.Journal of clinical medicine · 2025Review
- Age-related neutrophil activation in Hermansky-Pudlak Syndrome Type-1.Orphanet journal of rare diseases · 2025Article
- High fat diet feeding impairs neutrophil phagocytosis, bacterial killing, and neutrophil-induced hematopoietic regeneration.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Ferroptosis in idiopathic pulmonary fibrosis: mechanisms, impact, and therapeutic opportunities.Frontiers in immunology · 2025Review
- Neutrophils as key drivers of pulmonary fibrosis: unveiling mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- Review
- Opposite effects of systemic and local conditional CD11c+ myeloid cell depletion during bleomycin-induced inflammation and fibrosis in mice.Immunity, inflammation and disease · 2024Article
- Neutrophil dynamics in pulmonary fibrosis: pathophysiological and therapeutic perspectives.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Review
- Cell-Free DNA Maps Tissue Injury and Correlates with Disease Severity in Lung Transplant Candidates.American journal of respiratory and critical care medicine · 2024Article
- In vitro co-culture studies and the crucial role of fibroblast-immune cell crosstalk in IPF pathogenesis.Respiratory research · 2023Review
- PANoptosis: Mechanism and Role in Pulmonary Diseases.International journal of molecular sciences · 2023Review
- Disease progression in patients with usual interstitial pneumonia and probable UIP patterns on computed tomography with various underlying etiologies: a retrospective cohort study.Frontiers in medicine · 2023Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive, irreversible disease characterized by collagen deposition within the interstitium of the lung. This impairs gas exchange and results in eventual respiratory failure. Clinical studies show a correlation between elevated neutrophil numbers and IPF disease progression; however, the mechanistic roles neutrophils play in this disease are not well described. In the present study, we describe alterations to the trafficking and function of neutrophils after the development of fibrosis. We observed increased numbers of total and aged neutrophils in peripheral tissues of fibrotic mice. This appeared to be driven by an upregulation of neutrophil chemokine Cxcl2 by lung cells. In addition, neutrophil recruitment back to the bone marrow for clearance appeared to be impaired, because we saw decreased aged neutrophils in the bone marrow of fibrotic mice. Neutrophils in fibrosis were activated, because ex vivo assays showed increased elastase and extracellular trap release by neutrophils from fibrotic mice. This likely mediated disease exacerbation, because mice exhibiting a progressive disease phenotype with greater weight loss and mortality had more activated neutrophils and increased levels of extracellular DNA present in their lungs than did mice with a nonprogressive disease phenotype. These findings further our understanding of the dynamics of neutrophil populations and their trafficking in progressive fibrotic lung disease and may help inform treatments targeting neutrophil function for patients with IPF experiencing disease exacerbation in the future.
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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.