ArticleArthritis research & therapy2022
Neutrophil activation in patients with anti-neutrophil cytoplasmic autoantibody-associated vasculitis and large-vessel vasculitis.
Article in Arthritis research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- S100 proteins in IgA vasculitis and other systemic vasculitides - from pathogenic mechanisms to clinical biomarkers: a systematic review.Frontiers in immunology · 2026Pooled it
- Effects of Melatonin andAntioxidants (Basel, Switzerland) · 2026Article
- Role of neutrophils in regulating vascular permeability in inflammatory and autoimmune diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- N-formyl methionine peptide-driven neutrophil activation in idiopathic inflammatory myopathies.Rheumatology (Oxford, England) · 2026Article
- The role of NETosis in breast cancer: mechanistic insights and biomarker potential.Breast cancer research : BCR · 2025Review
- Uncovering the New Biology of Giant Cell Arteritis to Guide Therapeutic Strategies.Journal of clinical medicine · 2025Review
- Mitochondrial-Mediated Platelet Activation in Polymyalgia Rheumatica.ACR open rheumatology · 2025Article
- The role of calprotectin in giant cell arteritis - from pathophysiology to possible clinical applications.Frontiers in immunology · 2025Review
- A Glimpse into Humoral Response and Related Therapeutic Approaches of Takayasu's Arteritis.International journal of molecular sciences · 2024Review
- Review
- Review
- Mitochondrial N-formyl methionine peptides contribute to exaggerated neutrophil activation in patients with COVID-19.Virulence · 2023Article
- Distinguishing laboratory characteristics in giant cell arteritis: a real-world retrospective cohort study.International ophthalmology · 2023Article
- Mitochondrial-mediated inflammation and platelet activation in giant cell arteritis.Clinical immunology (Orlando, Fla.) · 2023Article
- Serum calprotectin and renal function decline in ANCA-associated vasculitides: a post hoc analysis of MAINRITSAN trial.RMD open · 2023Article
- Immune complex-mediated neutrophil activation in patients with polymyalgia rheumatica.Rheumatology (Oxford, England) · 2023Article
- The Emerging Role of Mitochondrial Dysfunction in the Pathogenesis of Idiopathic Inflammatory Myopathies.Rambam Maimonides medical journal · 2023Review
- Neutrophil extracellular trap formation in anti-neutrophil cytoplasmic antibody-associated and large-vessel vasculitis.Clinical immunology (Orlando, Fla.) · 2023Article
- Rs867228 in FPR1 accelerates the manifestation of luminal B breast cancer.Oncoimmunology · 2023Article
- Pathogenesis of giant cell arteritis with focus on cellular populations.Frontiers in medicine · 2022Review
Corrections and comments
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Authors and funding
19 authors at 13 institutions in 2 countries.
Funding
Abstract
objectiveTo assess markers of neutrophil activation such as calprotectin and N-formyl methionine (fMET) in anti-neutrophil cytoplasmic autoantibody-associated vasculitis (AAV) and large-vessel vasculitis (LVV).
methodsLevels of fMET, and calprotectin, were measured in the plasma of healthy controls (n=30) and patients with AAV (granulomatosis with polyangiitis (GPA, n=123), microscopic polyangiitis (MPA, n=61)), and LVV (Takayasu's arteritis (TAK, n=58), giant cell arteritis (GCA, n=68)), at times of remission or flare. Disease activity was assessed by physician global assessment. In vitro neutrophil activation assays were performed in the presence or absence of formyl peptide receptor 1 (FPR1) inhibitor cyclosporine H.
resultsLevels of calprotectin, and fMET were elevated in patients with vasculitis as compared to healthy individuals. Levels of fMET correlated with markers of systemic inflammation: C-reactive protein (r=0.82, p<0.0001), and erythrocyte sedimentation rate (r=0.235, p<0.0001). The neutrophil activation marker, calprotectin was not associated with disease activity. Circulating levels of fMET were associated with neutrophil activation (p<0.01) and were able to induce de novo neutrophil activation via FPR1-mediated signaling.
conclusionCirculating fMET appears to propagate neutrophil activation in AAV and LVV. Inhibition of fMET-mediated FPR1 signaling could be a novel therapeutic intervention for systemic vasculitides.
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