ArticleBioscience reports2020
Neutrophil extracellular trap from Kawasaki disease alter the biologic responses of PBMC.
Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- The Autophagy-Inflammasome Axis as a Molecular Switch: From Persistent Inflammation to Vascular Remodeling in IVIG-Resistant Kawasaki Disease.International journal of molecular sciences · 2026Review
- [Gut-vascular axis in Kawasaki disease: short-chain fatty acid-mediated immune regulation and therapeutic targets].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026Review
- Similarity of immune-associated markers in COVID-19 and Kawasaki disease: analyses from bioinformatics and machine learning.BMC pediatrics · 2025Article
- Neutrophils in tumor- and inflammation-induced lymphangiogenesis.International journal of biological sciences · 2025Review
- Integrated Bioinformatics Exploration and Preliminary Clinical Verification for the Identification of Crucial Biomarkers in Severe Cases of COVID-19.Journal of inflammation research · 2024Article
- Role of Neutrophil Extracellular Traps in Health and Disease Pathophysiology: Recent Insights and Advances.International journal of molecular sciences · 2023Review
- Identification of key signaling pathways and hub genes related to immune infiltration in Kawasaki disease with resistance to intravenous immunoglobulin based on weighted gene co-expression network analysis.Frontiers in molecular biosciences · 2023Article
- Cardiovascular involvement in Epstein-Barr virus infection.Frontiers in immunology · 2023Review
- Identifying differentially expressed genes and miRNAs in Kawasaki disease by bioinformatics analysis.Scientific reports · 2022Article
- Advances in understanding Kawasaki disease-related immuno-inflammatory response and vascular endothelial dysfunction.Pediatric investigation · 2022Review
- Human Transcriptome Array Analysis Identifies CDR2 as a Novel Suppressed Gene for Kawasaki Disease.Diagnostics (Basel, Switzerland) · 2022Article
- Mechanisms of Immune Dysregulation in COVID-19 Are Different From SARS and MERS: A Perspective in Context of Kawasaki Disease and MIS-C.Frontiers in pediatrics · 2022Review
- Detection of Extracellular Traps in Canine Steroid-Responsive Meningitis-Arteritis.Frontiers in veterinary science · 2022Article
- Extracellular traps and the role in thrombosis.Frontiers in cardiovascular medicine · 2022Review
- The role of mitochondria in the pathogenesis of Kawasaki disease.Frontiers in immunology · 2022Article
- CD177, a specific marker of neutrophil activation, is associated with coronavirus disease 2019 severity and death.iScience · 2021Article
- The Emerging Role of Neutrophils in the Pathogenesis of Thrombosis in COVID-19.International journal of molecular sciences · 2021Review
- Association Between rs12037447, rs146732504, rs151078858, rs55723436, and rs6094136 Polymorphisms and Kawasaki Disease in the Population of Polish Children.Frontiers in pediatrics · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kawasaki disease (KD), also known as mucocutaneous lymph node syndrome, is an acute systemic vasculitis syndrome that mainly occurs in infants under 5 years of age. In the current manuscript, we were aiming to analyze the role of neutrophil extracellular traps (NETs) in the pathogenesis of KD, especially their interplay with peripheral blood mononuclear cells (PBMCs). Neutrophils were exposed to 20 nM phorbol myristate acetate (PMA), we found that neutrophils of KD patients were more likely to form NETs compared with healthy controls (HCs). Furthermore, PBMCs were cultured with NETs for 24 h, and we observed that NETs significantly increased the cell viability, suppressed cell apoptosis, and enhanced the pro-inflammatory cytokines production and NF-κB activation in PBMCs from KD patients. In addition, with the stimulation of NETs, the expression of vascular endothelial growth factor A (VEGF-A) and hypoxia-inducible factor-1α (HIF-1α) were increased, which were related with the pathological mechanism of KD. At last, we examined the activation of phosphoinositide 3 kinase (PI3K)/Akt signaling, and we found NETs treatment obviously enhanced the activation of PI3K and Akt. In conclusion, these findings suggested that the formation of NETs may alter the biologic responses of PBMC and affect the vascular injury in KD.
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