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RANTES、单核细胞趋化蛋白-1及巨噬细胞炎性蛋白-1β在川崎病中表达的证据

Evidence for RANTES, monocyte chemotactic protein-1, and macrophage inflammatory protein-1 beta expression in Kawasaki disease.

作者信息

Wong M, Silverman E D, Fish E N

机构信息

Department of Medical Genetics and Microbiology, Faculty of Medicine, University of Toronto, Canada.

出版信息

J Rheumatol. 1997 Jun;24(6):1179-85.

PMID:9195529
Abstract

OBJECTIVE

Patients with Kawasaki disease mount an immune response directed to their abnormally stimulated vascular endothelium, that is associated with vascular inflammation and injury and a predisposition to arterial aneurysm formation. This suggests that specific pro-inflammatory cytokines may mediate these hyperreactive responses. The selective chemoattractant and activation effects of chemokines on lymphocytes identifies them as potential candidates in mediating selective inflammatory processes in Kawasaki disease. We examined peripheral blood from patients with Kawasaki disease for chemokine gene expression.

METHODS

Consecutive samples from 14 patients during the acute, subacute, and convalescent phases of their illness were collected and elaborated for RANTES, macrophage inflammatory protein-1 beta (MIP-1 beta) and monocyte chemotactic protein-1 (MCP-1) expression.

RESULTS

RANTES and MCP-1 gene expression levels were significantly elevated in 12 of the 14 patients, and MIP-1 beta gene expression was elevated in 13 of the 14 patients. There was no obvious correlation between clinical phase of the disease and chemokine expression level, yet elevated expression levels were detected in all phases, including the convalescent phase, when laboratory evidence of lymphocyte activation has been shown to return to normal. Serial samples showed persistence or increased expression of chemokine genes into the convalescent phase in patients with coronary artery lesions.

CONCLUSION

Chemokine mediated inflammatory events may persist in the convalescent phase of Kawasaki disease and may contribute to further risk of vascular endothelial cell injury, specifically coronary aneurysm formation.

摘要

目的

川崎病患者会对其异常激活的血管内皮产生免疫反应,这种反应与血管炎症和损伤以及动脉动脉瘤形成的易感性相关。这表明特定的促炎细胞因子可能介导这些高反应性反应。趋化因子对淋巴细胞的选择性趋化和激活作用表明它们可能是介导川崎病选择性炎症过程的潜在候选者。我们检测了川崎病患者外周血中趋化因子基因的表达情况。

方法

收集了14例患者在疾病急性期、亚急性期和恢复期的连续样本,并对其进行RANTES、巨噬细胞炎性蛋白-1β(MIP-1β)和单核细胞趋化蛋白-1(MCP-1)表达情况的详细检测。

结果

14例患者中有12例的RANTES和MCP-1基因表达水平显著升高,14例患者中有13例的MIP-1β基因表达升高。疾病的临床阶段与趋化因子表达水平之间没有明显的相关性,但在所有阶段,包括恢复期,当淋巴细胞激活的实验室证据已恢复正常时,仍检测到表达水平升高。连续样本显示,有冠状动脉病变的患者在恢复期趋化因子基因持续表达或表达增加。

结论

趋化因子介导的炎症事件可能在川崎病恢复期持续存在,并可能导致血管内皮细胞进一步损伤的风险增加,特别是冠状动脉瘤的形成。

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