Mechanism of coronary artery damage in Kawasaki disease and therapy

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Kawasaki disease (KD) is characterized by diffuse vasculitis including coronary artery aneurysm and marked immune activation such as high levels of tumor necrosis factor (TNF). To confirm possible mechnisms of injury to human coronary artery eridothelial cells (HCAEC) we invastigated expression of adhesion molecules on HCAEC as well as human umbilical vein endothelial cells (HUVEC) and production of chemokine by these endothelial cells following exposure to TNE.Levels of soluble E-selection and soluble intercellular adhesion molecule- 1 (ICAM- 1) were significantiy higher in sera from patients with KD than in normal controls. Monocyte chemoattractant protein- 1 (MCP- 1 ) and interleukin-8 (IL-8) were significantly higher in KD sera than in normal controls. TNF was able to increase E-selectin and ICAM- I on endothelial cells, and induce the production of MCP-1 and IL-8. These findings were remarkably recognized in HUAEC.ln summary, HCAEC activated by TNF remarkably expressed adhesion molecules and produced chemokine, resuting leukocyte accumulation in coronary artery endothelium. These findings suggest that abnormal activation of HEAEC may contributeto the development of coronary artery lesions inKD.