Investigation for the etiologic agents of Kawasaki syndrome using Protein Chip analysis

利用蛋白质芯片分析研究川崎综合征的病因

基本信息

批准号：
17591099
负责人：
NOMURA Yuichi
金额：
$ 2.05万
依托单位：
Kagoshima University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2005
资助国家：
日本
起止时间：
2005 至 2006
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-17591099/
关键词：
Kawasaki syndrome Protein Chip super antigen TSST-1

项目摘要

In order to find the etiologic agents of Kawasaki syndrome (KS), we investigated the serum protein profiles of patients with KS. Patients and Methods: Sera of 8 KS patients before treatment and 8 age matched febrile patients were used. To simplify the analysis conditions, these sera were collected from the KS patients at an early phase of the disease and younger than 6 months of age. Results: Among 250 peaks with an observed significant difference between KS and control patients, 20 peaks were selected as potential biomarkers. Two proteins were considered to represent 11 increased peaks observed in different conditions in the sera of KS patients; peak with mass-to-charge ratios (m/z): 11,524 and 11,581 in the cation exchange chip (pH4). These peak intensities in KS showed no correlation with the day of illness, number of KS symptoms, white blood cell counts, values of C-reactive protein, or values of transaminases. Among 9 decreased peak in KS, a peak with m/z 28,008 in the copper chip (pH7) showed the widest ROC area. These peaks were considered potential biomarkers of KS.Then, to confirm this fact, we investigated the serum protein profiles using another samples (sera of 8 KS patients and 5 controls). Results: There were no differences between KS and control groups in the peaks of m/z 11,524 or 11,631 in the cation exchange chip (pH4). However, using 16 KS samples and 13 control samples, peaks with m/z 17389, 17,405, 14,052, 8,702, and 14,056 in the cation exchange chip (pH4) were significantly different between the groups. In these peaks, there were peaks that elevated in the acute phase of KS.Conclusions; Although etiologic agents of KS were not detected, candidates for biomarkers of KS have been selected. Further examination is necessary.

为了找到川崎综合征（KS）的病因学剂，我们研究了KS患者的血清蛋白谱。患者和方法：使用治疗前8 KS患者的血清和8岁年龄匹配的发热患者。为了简化分析条件，这些血清是在疾病早期和6个月以下的早期阶段从KS患者那里收集的。结果：在250个峰和对照患者之间存在显着差异的峰中，选择了20个峰作为潜在的生物标志物。在KS患者的血清中，在不同条件下观察到的两种蛋白质代表了11个增加的峰。质量与电荷比（m/z）的峰值：阳离子交换芯片中的11,524和11,581。 KS中的这些峰值强度与疾病当天，KS症状的数量，白细胞计数，C反应性蛋白质值或转氨酶的值无关。在KS中的9个峰值中，铜芯片（pH7）中有M/z 28,008的峰值显示最宽的ROC面积。这些峰被认为是Ks.ss的潜在生物标志物，以确认这一事实，我们使用其他样品（血清8 KS患者和5个对照组）研究了血清蛋白谱。结果：在阳离子交换芯片中，KS和对照组之间的KS和对照组之间没有差异（PH4）。但是，使用16 ks样品和13个对照样品，两组的阳离子交换芯片（PH4）中具有m/z 17389、17,405、14,052、8,702和14,056的峰值显着不同。在这些峰值中，在KS.结论的急性阶段升高了峰。尽管未检测到KS的病因学剂，但已选择了KS生物标志物的候选物。需要进一步检查。