ArticleResearch and practice in thrombosis and haemostasis2024
Platelets from patients with chronic inflammation have a phenotype of chronic IL-1β release.
Article in Research and practice in thrombosis and haemostasis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Chemical Profiling and Anti-Inflammatory Mechanisms ofMetabolites · 2026Article
- Platelets in systemic lupus erythematosus: from hemostatic allies to pathogenic drivers.Frontiers in immunology · 2026Review
- Association of systemic immune-inflammation index (SII) with epigenetic age acceleration in adults: insights from NHANES.Epigenetics · 2025Article
- Review
- Neutrophils and Platelets as Key Players in the Pathogenesis of ANCA-Associated Vasculitis and Potential Sources of Disease Activity Biomarkers.Diagnostics (Basel, Switzerland) · 2025Review
- Anti-Inflammatory Actions of Plant-Derived Compounds and Prevention of Chronic Diseases: From Molecular Mechanisms to Applications.International journal of molecular sciences · 2025Review
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Chronic inflammation is a cardiovascular risk factor, and interleukin-1β (IL-1β) is central to the inflammatory host response. Platelets contain the NLRP3 inflammasome and are able to translate IL-1β messenger RNA (mRNA) and secrete mature IL-1β upon activation. However, the role of a chronic inflammatory environment in platelet IL-1β mRNA and protein content remains unclear. Objectives: The aim of the current study was to investigate intracellular platelet IL-1β and IL-1β mRNA in a chronic inflammatory state. Methods: Sixty-five patients with stable inflammation (ie, high-sensitivity C-reactive protein within predefined margins in 2 separate measurements) were stratified according to high-sensitivity C-reactive protein levels in low (0.0-0.9 mg/L), medium (1.0-2.9 mg/L), and high (3.0-9.9 mg/L) risk groups. Platelet reactivity as well as platelet IL-1β protein synthesis were studied. Results: The highest risk group was characterized by a distinct cardiovascular risk profile and approximately 20% higher platelet counts. While platelet reactivity was not different, a reduction in intracellular platelet IL-1β mRNA and IL-1β protein levels was observed in the highest risk group and was linked to decreased platelet size and granularity. This signature suggests a phenotype of chronic IL-1β secretion and could be experimentally phenocopied by stimulation of platelets from healthy volunteers with either TRAP-6 or collagen related peptide (CRP-XL). Conclusion: Our data suggest a phenotype of chronic IL-1β secretion by platelets in patients with chronic sterile inflammation.
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