摘要
目的观察川崎病(KD)患儿急性期血清和丙种球蛋白对单核巨噬细胞Toll样受体4(TLR4)信号传导途径分子基因表达的影响,以探讨TLR4信号传导途径在KD血管损伤过程中的作用及丙种球蛋白治疗KD可能的作用机制。方法急性期KD患儿40例,健康对照组10例。分别用KD患儿急性期血清和KD急性期血清加丙种球蛋白作用于佛波酯诱导分化的人单核巨噬细胞(THP-1),采用反转录-PCR(RT-PCR)检测不同实验条件作用下的THP-1中TLR4信号途径传导分子mRNA的表达情况。结果急性期KD患儿血清刺激巨噬细胞表达TLR4 mRNA、MyD88 mRNA、TNF受体相关因子6(TRAF6)mRNA明显高于健康对照组;而加入丙种球蛋白后可显著抑制KD并冠状动脉损伤(CAL)血清组(KD-CAL+组)mRNA的表达;而KD无CAL血清组(KD-CAL-组)与KD-CAL+组比较,巨噬细胞TLR4 mRNA、MyD88 mRNA、TRAF6 mRNA、CD14mRNA的表达量无明显差异。结论 TLR4-MyD88途径参与KD免疫功能紊乱及血管炎性损伤过程,而丙种球蛋白作用于TLR4-MyD88途径可能为治疗KD的机制之一。
Objective To evaluate the gene expression of several molecules in Toll-like-receptor-4（TLR4） signal transduction pathway in the monocytes /macrophages after getting stimulated by the serum of Kawasaki disease（KD） patients in the acute phase as well as by γ-globulin,and to investigate the role of TLR4 in endothelial damage of KD and possible mechanism of γ-globulin in the treatment of KD.Methods Forty children with KD and 10 cases age-matched healthy children were studied.The gene expression of several molecules in TLR4 signal transduction pathway in the monocytes macrophages was evaluated after getting stimulated by the serum of KD patients in the acute phase as well as by γ-globulin.Results The expressions of TLR4 mRNA,MyD88 mRNA,TRAF6 mRNA in the human mononuclear macrophage（THP-1） were upregulated in KD serum group than in healthy control group,and γ-globulin could abolish the effect of KD serum group on TLR4 mRNA,MyD88 mRNA,and TRAF6 mRNA expressions;there was no difference in TLR4 mRNA,MyD88 mRNA,TRAF6 mRNA and CD14 mRNA expressions between KD-non coronary artery damage（KD-CAL-） serum group and KD-coronary artery damage（KD-CAL^＋） serum group.Conclusions It is assumed that TLR4 pathway involves in vascular damage in KD,and blocking the TLR4 pathway may be one of the mechanisms of γ-globulin to treat KD.
出处
《实用儿科临床杂志》
CAS
CSCD
北大核心
2010年第21期1631-1633,共3页
Journal of Applied Clinical Pediatrics
