Key result
High systemic inflammation (hs-CRP 3.0-9.9 mg/L) was associated with reduced intracellular platelet IL-1β mRNA and protein levels, suggesting a phenotype of chronic IL-1β secretion.
Why the study?
The role of a chronic inflammatory environment in platelet IL-1β mRNA and protein content remains unclear.
Cross-Sectional (n=65)
Patients with chronic sterile inflammation exhibit a platelet phenotype characterized by chronic IL-1β secretion, which may contribute to cardiovascular risk.
May indicate chronic platelet IL-1β secretion in high hs-CRP; hypothesis-generating for CV risk and requires prospective validation.
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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Berger et al. (2023) conducted a cross-sectional in Chronic inflammation (n=65). High systemic inflammation (hs-CRP 3.0-9.9 mg/L) vs. Low (0.0-0.9 mg/L) and medium (1.0-2.9 mg/L) systemic inflammation was evaluated on Intracellular platelet IL-1β mRNA and IL-1β protein levels. High systemic inflammation (hs-CRP 3.0-9.9 mg/L) was associated with reduced intracellular platelet IL-1β mRNA and protein levels, suggesting a phenotype of chronic IL-1β secretion.
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