ArticleArthritis research & therapy2019
Increased neutrophil extracellular traps activate NLRP3 and inflammatory macrophages in adult-onset Still's disease.
Article in Arthritis research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.
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Who cites it
89 citing papers in PubMed, 1 synthesis or guideline pooled it, 122 citations in OpenAlex.
- Stress and circulating cell-free mitochondrial DNA: A systematic review of human studies, physiological considerations, and technical recommendations.Mitochondrion · 2021Pooled it
- Urinary Proteomics Identifying Novel Biomarkers for the Diagnosis of Adult-Onset Still's Disease.Frontiers in immunology · 2020Trial
- Low-Density Granulocytes Link to Disease Activity, Organ Involvement, and Cytokine Production in Sjögren's Disease.International journal of molecular sciences · 2026Article
- Neutrophil extracellular traps promote macrophage activation through Toll-like receptor engagement and PKA and NF-kB signaling pathways.Cell communication and signaling : CCS · 2026Article
- Pathogenic and genetic landscape of Still's disease across ages, with new insights into age-related IL-18 patterns.Arthritis research & therapy · 2026Review
- Rethinking Mitochondria: The Extracellular Dimension.Circulation research · 2026Review
- Still's Disease and Autoinflammation: Positioning an Inflammatory Syndrome on the Autoinflammation-Autoimmunity Spectrum.Current rheumatology reports · 2026Review
- Fuzheng Jiedu formula attenuates acute pneumonia by coordinated regulation of macrophage NLRP3 inflammasome and neutrophil NETs.Chinese medicine · 2026Article
- Association of elevated serum active IL-18 levels with cytokine profiles and clinical features in adult-onset still's disease.Frontiers in immunology · 2026Article
- Neutrophil extracellular trap-associated responses are associated with tissue factor expression and coagulation abnormalities during anaphylaxis.Frontiers in immunology · 2026Article
- Review
- TLR9 decreases FOXO3 expression to prevent excessive inflammation in macrophage activation syndrome.iScience · 2025Article
- Anti-β2glycoprotein I-induced neutrophil extracellular traps cause endothelial activation.Rheumatology (Oxford, England) · 2025Article
- Inflammasomes in Cardiovascular Diseases: Current Knowledge and Future Perspectives.International journal of molecular sciences · 2025Review
- High Neutrophil Alkaline Phosphatase Activity in Adult-Onset Still's Disease.Rheumatology and therapy · 2025Article
- Article
- Review
- The emerging role of neutrophil extracellular traps in autoimmune and autoinflammatory diseases.MedComm · 2025Review
- NLRP3 Inflammasome Activation Modulates Neutrophil Extracellular Trap Formation and Aggravates Airway Inflammation in Bronchiectasis.Research (Washington, D.C.) · 2025Article
- Neutrophil extracellular traps and interleukin-1β in cystic fibrosis lung disease.Frontiers in immunology · 2025Review
29 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAdult-onset Still's disease (AOSD) is a systemic inflammatory disease characterized by neutrophilia and NLRP3 inflammasome and macrophage activation. We investigated the role of neutrophil extracellular traps (NETs) in the pathogenesis of AOSD, and explored the effect of NETs on activating NLRP3 inflammasome and proinflammatory macrophages.
methodsThe sera of 73 AOSD patients and 40 healthy controls were used to detect the level of cell-free DNA and NET-DNA complexes. NET formation ex vivo was analyzed using immunofluorescence and flow plates. The activation of NLRP3 inflammasome in THP-1 cells and proinflammatory macrophages stimulated with DNA purified from NETs was measured using RT-PCR, ELISA, Western blotting and flow cytometry.
resultsThe levels of cell-free DNA and NET-DNA complexes were significantly increased in the circulation of patients with AOSD compared with healthy controls, and freshly isolated neutrophils from patients with AOSD were predisposed to high levels of spontaneous NET release. Interestingly, enhanced NET release was abrogated with NADPH oxidase inhibitors and a mitochondrial scavenger. Furthermore, DNA purified from AOSD NETs activated NLRP3 inflammasomes. NET DNA from AOSD also exerted a potent capacity to accelerate the activation of CD68
conclusionsThese findings implicate accelerated NET formation in AOSD pathogenesis through activation of NLRP3 and proinflammatory macrophages, and identify a novel link between neutrophils and macrophages by NET formation in AOSD.
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