白三烯B4-白三烯B4受体2通路在川崎病血管损伤发生机制中的作用

Role of leukotriene B4-BLT2 pathway in the mechanism of endothelial damage in Kawasaki disease

目的观察川崎病（KD）急性期血清和丙种球蛋白对血管内皮细胞产生白三烯B4（LTB4）的影响，以及不同刺激后的内皮细胞条件培养基对单核巨噬细胞表达LTB4受体2（BLIT2）的影响，以了解LTB4-BLT2通路在KD血管损伤过程中的作用以及丙种球蛋白治疗KD可能的作用机制。方法分别用KD急性期血清和KD急性期血清加丙种球蛋白作用于人脐静脉内皮细胞（ECV304）后，酶联免疫吸附试验（ELISA）检测内皮细胞条件培养基中LTB4浓度的改变；用流式细胞术检测不同内皮细胞条件培养基作用于单核巨噬细胞后，巨噬细胞表达BLT2的情况。结果KD血清能够诱导内皮细胞产生LTB4，KD血清刺激后的内皮细胞条件培养基能够使巨噬细胞BLT2表达上调；而加入丙种球蛋白后可显著抑制上述LTB4和BLT2的改变。结论LTB4-BLIT2通路参与KD血管炎性损伤过程，丙种球蛋白阻断LTB4-BLT2通路可能是其抗KD冠状动脉损伤的机制之一。

Objective To investigate the effect of the serum of patients with acute Kawasaki disease （KD） and v-globulin on endothelial cell-produced leukotriene B4 （LTB4）. Meanwhile, the effects of the endothelial cell conditioned culture media （ECM） on the expression of BLT2 in macrophage were observed. The purpose of this study is to understand whether LTB4-BLT2 pathway is involved in endothelial damage in KD and the mechanism of γ-globulin in the treatment of KD. Methods We measured the LTB4 concentration in cell culture after stimulated by serum of KD patients and γ-globulin. The expression of BLT2 in the macrophage was determined by flow cytometry. Results The serum of patients with KD increased the concentration of LTB4 in the endothelial cell culture （P〈0.01 vs normal control）. The expression of BLT2 in the macrophage was enhanced significantly （P〈0.01 vs normal control）, But γ-globulin did not have these effects. Conclusion The result of this study suggests that LTB4-BLT2 pathway may be involved in vascular damage in KD, and the mechanism of γ-globulin in managing KD may be related to blocking the LTB4-BLT2 pathway.