ArticleClinical and translational science2023
Neutrophil elastase activates the release of extracellular traps from COPD blood monocyte-derived macrophages.
Article in Clinical and translational science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 13 citations in OpenAlex.
- MLKL regulates intracellular trafficking of neutrophil elastase to promote lung epithelial cell senescence.American journal of respiratory cell and molecular biology · 2026Article
- UBE2M deficiency in alveolar macrophages promotes emphysema through HIF-2α/MMP12 axis.Chinese medical journal pulmonary and critical care medicine · 2026Article
- Macrophage Extracellular Traps in Immunity and Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Convergent death programs in chronic obstructive pulmonary disease: how pyroptotic and ferroptotic crosstalk reshapes therapeutic paradigms.Frontiers in immunology · 2026Review
- Correlations Between Inflammatory Biomarkers and COPD Severity in a Real-Life Setting.Journal of clinical medicine · 2025Article
- Exploring the Role of Macrophages and Their Associated Structures in Rheumatoid Arthritis.Journal of innate immunity · 2025Review
- Urine Neutrophil Elastase: A Novel Predictor of ICU Admission for Patients with COVID-19 Infection.Journal of inflammation research · 2025Article
- Development and validation of a nomogram for predicting bacterial infections in patients with acute exacerbation of chronic obstructive pulmonary disease.Experimental and therapeutic medicine · 2025Article
- Neutrophil Elastase Targets Select Proteins on Human Blood-Monocyte-Derived Macrophage Cell Surfaces.International journal of molecular sciences · 2024Article
- Aromadendrin Ameliorates Airway Inflammation in Experimental Mice with Chronic Obstructive Pulmonary Disease.Journal of microbiology and biotechnology · 2024Article
- Neutrophil Elastase Degrades Histone Deacetylases and Sirtuin 1 in Primary Human Monocyte Derived Macrophages.International journal of molecular sciences · 2024Article
- Neutrophil elastase activates the release of extracellular traps from COPD blood monocyte-derived macrophages.Clinical and translational science · 2023Article
- Bronchiectasis-COPD Overlap Syndrome: A Comprehensive Review of its Pathophysiology and Potential Cardiovascular Implications.Therapeutic advances in pulmonary and critical care medicineReview
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophil elastase (NE), a major inflammatory mediator in chronic obstructive pulmonary disease (COPD) airways, impairs macrophage function, contributing to persistence of airway inflammation. We hypothesized that NE activates a novel mechanism of macrophage-induced inflammation: release of macrophage extracellular traps (METs). The METs are composed of extracellular DNA decorated with granule proteinases and oxidants and may trigger persistent airway inflammation in COPD. To test the hypothesis, human blood monocytes were isolated from whole blood of subjects with COPD recruited following informed written consent. Patient demographics and clinical data were collected. Cells were cultured in media with GM-CSF to differentiate into blood monocyte derived macrophages (BMDMs). The BMDMs were treated with FITC-NE and unlabeled NE to determine intracellular localization by confocal microscopy and intracellular proteinase activity by DQ-Elastin assay. After NE exposure, released extracellular traps were quantified by abundance of extracellular DNA in conditioned media using the Pico Green assay. BMDM cell lysates were analyzed by Western analysis for proteolytic degradation of histone H3 or H4 or upregulation of peptidyl arginine deiminase (PAD) 2 and 4, two potential mechanisms to mediate extracellular trap DNA release. We observed that NE was taken up by COPD BMDM, localized to the cytosol and nucleus, and retained proteinase activity in the cell. NE induced MET release at doses as low as 50 nM. NE treatment caused histone H3 clipping but no effect on histone H4 nor PAD 2 or 4 abundance or activity. In summary, NE activated COPD MET release by clipping histone H3, a prerequisite for chromatin decondensation.
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