Neutrophil expression of CD41/CD61 complex contributes to their adhesiveness in both healthy individuals and heart failure patients

Neutrophils can release pro-inflammatory cytokines and neutrophil extracellular traps (NETs), leading to vascular thrombosis. Neutrophil-platelet interaction, a major component of thrombosis, is more pronounced in inflammatory pathologies, such as heart failure (HF). Recently, the platelet receptor CD41/CD61 (GPIIb/IIIa), known for its role in platelet adhesion and aggregation via its binding to fibrinogen, was found on the membrane of neutrophils from lung cancer patients. Our objectives were to determine CD41/CD61 expression on neutrophils and its role in healthy volunteers (HV) and acute decompensated heart failure patients (ADHF). Localization and expression of CD41/CD61 complex on isolated neutrophils were determined by flow cytometry and confocal microscopy. We assessed the CD41/CD61 role on neutrophil adhesion onto human extracellular matrix (hECM), NETosis and release of inflammatory cytokines. CD41/CD61 complex was intracellularly expressed in 80–90% of neutrophils, but only between 8 and 13% on their extracellular membrane. The CD41/CD61 complex plays a role in neutrophil adhesion onto hECM, since its blockade by an anti-CD41 monoclonal antibody or its antagonist, eptifibatide, reduced CXCL8 and PMA induced neutrophil adhesion from 52 to 100% in both HV and ADHF patients. In summary, neutrophil specific CD41/CD61 expression contributes to neutrophil adhesiveness without affecting significantly the release of inflammatory cytokines and NETosis in both HV and ADHF patients.