Platelets from patients with chronic inflammation have a phenotype of chronic IL-1® release.

Background Chronic inflammation is a cardiovascular risk factor and interleukin-1® (IL-1®) is central to the inflammatory host response. Platelets contain the NLRP3 inflammasome and are able to translate IL-1® mRNA and secrete mature IL-1® upon activation. However, the role of a chronic inflammatory environment on platelet IL-1® mRNA and protein content remains unclear. Methods Sixty-five patients with stable inflammation (i.e. hsCRP within predefined margins in 2 separate measurements) were stratified according to hsCRP levels in a low (0.0 – 0.9 mg/L), medium (1.0 – 2.9 mg/L) and high (3.0 – 9.9 mg/L) risk group. Platelet reactivity as well as platelet IL-1® protein synthesis was studied. Results The highest risk group was characterised by a distinct cardiovascular risk profile and approximately 20% higher platelet counts. While platelet reactivity was not different, a reduction of intracellular platelet IL-1® mRNA and IL-1® protein levels was observed in the highest risk group and linked to decreased platelet-size and granularity. This signature suggests a phenotype of chronic IL-1® 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 suggests a phenotype of chronic IL1β- secretion by platelets in patients with chronic sterile inflammation.