Background
Kawasaki disease (KD) is a systemic vasculitis syndrome that commonly occurs in children. Autophagy has been increasingly shown to be involved in various cardiovascular diseases, including endothelial dysfunction and vascular endothelial injury. However, whether autophagy is implicated in the pathogenesis of KD remains poorly understood, and particularly, how the dysfunction of human coronary artery endothelial cells (HCAECs) is associated with autophagy in peripheral blood mononuclear cells (PBMCs) from KD patients awaits further investigation.
Conclusions
Autophagy is involved in the inflammatory injury of vascular endothelial cells associated with PBMCs in KD patients, and may play a crucial role in regulating inflammation. Hence, we identify a novel regulatory mechanism of vascular injury in this disease.
Methods
Peripheral blood samples were collected from KD patients, common fever patients, and healthy controls. The PBMC samples were isolated from KD blood samples collected at three different phases: the acute phase before therapy (acute-KD), 1 week (subacute-KD), and 4 weeks (convalescent-KD) after drug administration.
Results
The autophagy flux was significantly increased in the PBMCs of KD patients at acute phase. The PBMCs of acute KD patients could induce autophagy in HCAECs and promote the secretion of chemokines and pro-inflammatory factors after cocultured with HCAECs whereas 3-methyladenine (3-MA) drug could partly reverse this process. Conclusions: Autophagy is involved in the inflammatory injury of vascular endothelial cells associated with PBMCs in KD patients, and may play a crucial role in regulating inflammation. Hence, we identify a novel regulatory mechanism of vascular injury in this disease.