Reverse regulation of soluble receptor for advanced glycation end products and proinflammatory factor resistin and S100A12 in Kawasaki disease

Introduction: Kawasaki disease (KD), an acute febrile disease, characterized by systemic vasculitis, predominantly affects infants and children under 5 years of age. Coronary artery lesions (CALs) are its most critical complication, and the etiology remains unknown yet. In order to explore the value of resistin, S100A12 and soluble receptor for advanced glycation end products (sRAGE) in the pathophysiology of KD, we studied the serum levels of resistin, S100A12 and sRAGE in different stages of KD. Methods: Serum levels of resistin, S100A12 and sRAGE were measured by enzyme-linked immunosorbent assay (ELISA) method in 15 healthy children and 40 KD patients at acute, afebrile and subacute stage. Results: The resistin and S100A12 levels, including the ratio of resistin to sRAGE and S100A12 to sRAGE increased significantly in the acute stage, and decreased progressively in the afebrile and subacute stage. However, the sRAGE levels decreased significantly in the acute stage, and increased progressively in the afebrile and subacute stage. In the acute, afebrile and subacute stage, the resistin levels were higher in intravenous immunoglobulin (IVIG) non-responders (0.64 +/- 0.30, 0.48 +/- 0.35, 0.28 +/- 0.19, x 10(2) ng/ml) than in IVIG responders (0.35 +/- 0.24, 0.21 +/- 0.19, 0.12 +/- 0.05, x 10 (2) ng/ml). In the acute and subacute stage, the S100A12 levels were higher in IVIG non-responders (7.92 +/- 2.61, 4.98 +/- 4.75, x 10 (2) ng/ml) than in IVIG responders (5.05 +/- 3.22, 2.35 +/- 2.26, x 10 (2) ng/ml). In the afebrile and subacute stage, the sRAGE levels were lower in IVIG non-responders (3.51 +/- 2.64, 3.65 +/- 3.27, x 10(2) pg/ml) than in IVIG responders (6.00 +/- 2.78, 7.19 +/- 2.88, x 10(2) pg/ml). The resistin levels were positively correlated with S100A12 levels. The sRAGE levels were negatively related with S100A12 and resistin levels. Conclusions: Resistin, S100A12 and sRAGE are involved in the pathophysiology of KD.