Circulating Platelet-Neutrophil Aggregates Play a Significant Role in Kawasaki Disease

injury may lead to increased platelet activation with neutrophil and monocyte infiltration, as well as increased platelet adhesion and aggregation via the release of inflammatory cytokines with mutually facilitated.8–10 Circulating platelet-neutrophil aggregates amplify acute inflammation and exhibit a hyper-reactive response that could promote the development of thrombotic and inflammatory disease, obstruct the flow of coronary microvessels, and contribute to vascular inflammation and tissue injury.11–13 Likewise, activated platelets and neutrophils have been demonstrated during the acute phase of KD-associated inflammation and may be contribute to the occurrence of CAA.14–17 Therapeutic inhibition of platelet-neutrophil aggregates reduces neutrophil recruitment and permeability and may help to attenuate organ damage and mitigate the inflammatory process.18–20 Prednisolone can cause the inhibition of platelet adhesion, spreading, aggregation, thrombus formation and the interaction of platelets with monocytes through regulaawasaki disease (KD) is an acute febrile illness characterized by systemic vasculitis, and may lead to coronary artery abnormalities (CAA).1,2 High-dose intravenous immunoglobulin (IVIG) treatment effectively resolves the inflammation and reduces the occurrence of CAA in patients with KD.3 However, approximately 10–20% of patients with KD have sustained or recurrent fever after IVIG, and are at risk of developing CAA.4 Primary treatment with a combination of IVIG plus prednisolone (PSL) recently showed a significant advantage over IVIG alone for the prevention of CAA, reducing the need for additional rescue treatments.5 Platelets are involved in hemostasis, wound healing, and inflammation. Platelet activation at the site of inflamed endothelium contributes to vascular inflammation and vascular wall remodeling. Released chemokine from activated platelets, such as platelet factor 4 (PF4), CXCL7 and β-thromboglobulin (β-TG), have important effects on vascular inflammation.6,7 Vascular K