ArticleInnate immunity2016
Neutrophil azurophilic granule exocytosis is primed by TNF-α and partially regulated by NADPH oxidase.
Article in Innate immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- Differential Regulation of Neutrophil Elastase Release vs. NET Generation After Cardiopulmonary Bypass.International journal of molecular sciences · 2026Article
- The Nox2 NADPH oxidase regulates neutrophilic inflammation in the oral cavity.Mucosal immunology · 2026Article
- Pervasive enhanced transcription in inflammatory breast cancer tumors and PBMCs impacts RNA splicing and intronic RNAs in plasma.Science advances · 2026Article
- Acidic pH promotes degranulation and reduces oxidative stress in human primary neutrophils.EXCLI journal · 2026Article
- Neutrophil Killing ofJournal of innate immunity · 2026Article
- Transforming Growth Factor-β1 Drives Neutrophil Chemokinesis, Not Chemotaxis.Journal of inflammation research · 2026Article
- Differential regulation of neutrophil degranulation by p38 MAPK and mitochondrial ROS duringFrontiers in pharmacology · 2026Article
- Activated neutrophils: A next generation cellular immunotherapy.Bioengineering & translational medicine · 2025Review
- Neutrophils and Anesthetic Drugs: Implications in Onco-Anesthesia.International journal of molecular sciences · 2024Review
- Article
- Evaluation of the innate immune response of caprine neutrophils against Mycobacterium avium subspecies paratuberculosis in vitro.Veterinary research · 2023Article
- Hyaluronan promotes intracellular ROS production and apoptosis in TNFα-stimulated neutrophils.Frontiers in immunology · 2023Article
- Dusp6 deficiency attenuates neutrophil-mediated cardiac damage in the acute inflammatory phase of myocardial infarction.Nature communications · 2022Article
- TREM-1 is required for enhanced OpZ-induced superoxide generation following priming.Journal of leukocyte biology · 2022Article
- Molecular Characterization of Kunitz-Type Protease Inhibitors from Blister Beetles (Coleoptera, Meloidae).Biomolecules · 2022Article
- Pseudomonas aeruginosa modulates neutrophil granule exocytosis in an in vitro model of airway infection.Immunology and cell biology · 2022Article
- Neutrophil Extracellular Trap Formation Potential Correlates with Lung Disease Severity in COVID-19 Patients.Inflammation · 2022Article
- Efficient Neutrophil Activation Requires Two Simultaneous Activating Stimuli.International journal of molecular sciences · 2021Article
- NETs in APS: Current Knowledge and Future Perspectives.Current rheumatology reports · 2020Review
- Therapeutic targeting of neutrophil exocytosis.Journal of leukocyte biology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Neutrophil (polymorphonuclear leukocyte) activation with release of granule contents plays an important role in the pathogenesis of acute lung injury, prompting clinical trials of inhibitors of neutrophil elastase. Despite mounting evidence for neutrophil-mediated host tissue damage in a variety of disease processes, mechanisms regulating azurophilic granule exocytosis at the plasma membrane, and thus release of elastase and other proteases, are poorly characterized. We hypothesized that azurophilic granule exocytosis would be enhanced under priming conditions similar to those seen during acute inflammatory events and during chronic inflammatory disease, and selected the cytokine TNF-α to model this in vitro. Neutrophils stimulated with TNF-α alone elicited intracellular reactive oxygen species (ROS) generation and mobilization of secretory vesicles, specific, and gelatinase granules. p38 and ERK1/2 MAPK were involved in these components of priming. TNF-α priming alone did not mobilize azurophilic granules to the cell surface, but did markedly increase elastase release into the extracellular space in response to secondary stimulation with N-formyl-Met-Leu-Phe (fMLF). Priming of fMLF-stimulated elastase release was further augmented in the absence of NADPH oxidase-derived ROS. Our findings provide a mechanism for host tissue damage during neutrophil-mediated inflammation and suggest a novel anti-inflammatory role for the NADPH oxidase.
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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.