Increase expression of CD177 in Kawasaki disease
Increase expression of CD177 in Kawasaki disease
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DOI：
10.1186/s12969-019-0315-8
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发表时间：
2019-04-03
影响因子：
2.5
通讯作者：
Kuo, Ho-Chang
中科院分区：
文献类型：
--
作者：
Huang, Ying-Hsien;Lo, Mao-Hung;Kuo, Ho-Chang
川崎病（Kawasaki disease，KD）是儿童最常见的急性冠状动脉炎性疾病.其发病率归因于感染、遗传和免疫的综合作用。虽然KD的发病机制仍然未知，我们已经进行了一项调查，全球遗传DNA甲基化状态和转录表达的KD患者，以确定其贡献的发病机制KD.MethodsWe招募了148名参与者的病例对照研究。芯片研究包括18名KD患者，在接受静脉注射免疫球蛋白（IVIG）治疗前和治疗后至少3周进行分析，以及36名非KD对照受试者，使用Illumina HumanMethylation 450 BeadChip和Affychip（R）Human Transcriptome Array 2.0。然后，我们进行了实时定量PCR的一个单独的队列94科目validation.ResultsAccording我们的微阵列研究，CD177，中性粒细胞表面分子，出现显着上调KD患者相比，控制表观遗传低甲基化。患者接受IVIG治疗后，CD177 mRNA水平明显下降。PCR验证表明CD177表达与Transcriptome Array 2.0结果一致。此外，KD患者与对照组之间CD 177的曲线下面积值为0.937。我们还观察到显着较高的CD 177水平在典型的KD比在不完全介绍或KD与IVIG resistance.ConclusionIn这项研究中，我们已经证明了表观遗传低甲基化和CD 177的表达增加在KD的急性期。此外，CD 177在典型表现的KD患者中的较高表达与IVIG抵抗相关。
BackgroundKawasaki disease (KD) is the most common acute coronary vasculitis disease to occur in children. Its incidence has been attributed to the combined effects of infection, genetics, and immunity. Although the etiopathogenesis of KD remains unknown, we have performed a survey of global genetic DNA methylation status and transcripts expression in KD patients in order to determine their contribution to the pathogenesis of KD.MethodsWe recruited 148 participants for this case-control study. The chip studies consisted of 18 KD patients that were analyzed both before undergoing intravenous immunoglobulin (IVIG) treatment and at least 3weeks afterward, as well as 36 non-KD control subjects, using Illumina HumanMethylation450 BeadChip and Affymetrix GeneChip (R) Human Transcriptome Array 2.0. We then carried out real-time quantitative PCR on a separate cohort of 94 subjects for validation.ResultsAccording to our microarray study, CD177, a neutrophil surface molecule, appeared to be significantly upregulated in KD patients when compared to controls with epigenetic hypomethylation. After patients received IVIG treatment, CD177 mRNA levels decreased significantly. PCR validation indicated that the CD177 expression is consistent with the Transcriptome Array 2.0 results. Furthermore, the area under the curve values of CD177 between KD patients and controls is 0.937. We also observed significantly higher CD177 levels in typical KD than in incomplete presentation or KD with IVIG resistance.ConclusionIn this study, we have demonstrated the epigenetic hypomethylation and increased expression of CD177 during the acute stage of KD. Furthermore, a higher expression of CD177 in KD patients with typical presentation was associated with IVIG resistance.