Inflammation, Platelets and Sickle Cell Disease

Pathophysiology of sickle cell disease is incompletely understood. The typical change of red blood cells into sickle cells lead to post-capillary stream abnormalities. This phenomenon is responsible of ischemia-reperfusion injuries. Chronic hemolysis is the second part of the pathophysiology. The consequences are vasoconstriction, endothelial lesions, chronic inflammation, hemostasis and platelets activation. Thrombo-inflammation concept was proposed by Tanguay to describe the interactions between hemostasis, platelets and innate immune cells (neutrophils polynuclear) during thrombotic process. Since this time, this concept was largely described in many clinical situations such as septicemia, COVID-19, coronaropathy, auto-immune diseases and sickle cell disease. In this project, we will study platelets activation and thrombo-inflammation markers in the beginning of a vaso-occlusive crisis, during the crisis and two months after the crisis. Blood samples will be collected during a routine care sample. Biological markers studied will be: * Soluble and surface markers of platelet activation; platelet-leukocytes aggregates * Plasmatic eicosanoids produced by platelets (TXB2) and immune cells * In vitro platelets reactivity; dynamic thrombus formation in normal and pathologic arterial blood stream * Platelet's inflammasome