Intravenous immunoglobulin (IVIG)-resistant Kawasaki disease (KD) is a complex disease, leading to the damage of multiple systems. The pathogen that triggers this sophisticated disease is still unknown. The aim of this study was to identify gene signatures during IVIG-resistant KD and uncover their potential mechanisms. The gene expression profiles of GSE18606 were downloaded from the GEO database. The GSE18606 dataset contained eight IVIG-resistant KD samples and nine healthy age-appropriate controls. The gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes pathway analyses were performed, and protein-protein interaction (PPI) network of the differentially expressed genes (DEGs) was constructed by Cytoscape software. In total, 73 DEGs were identified in IVIG-resistant KD, including 58 upregulated genes and 15 downregulated genes. GO analysis results showed that DEGs were significantly enriched in biological processes of neutrophil degranulation, neutrophil mediated immunity, and neutrophil activation involved in immune response. Among them, 10 hub genes (S100A8, S100A9, S100A12, HGF, LCN2, LY96, CTGF, MMP8, IRAK3, and SLPI) with a high degree of connectivity were selected. The present study indicated that the identified DEGs and hub genes promote our understanding of the molecular mechanisms underlying the development of IVIG-resistant KD, and might be used as molecular targets and diagnostic biomarkers for the treatment of IVIG-resistant KD.

中文翻译：

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使用生物信息学分析鉴定免疫球蛋白抗性川崎病的潜在核心基因。

静脉注射免疫球蛋白 (IVIG) 耐药的川崎病 (KD) 是一种复杂的疾病，会导致多个系统的损害。引发这种复杂疾病的病原体仍然未知。本研究的目的是确定 IVIG 抗性 KD 期间的基因特征并揭示其潜在机制。GSE18606的基因表达谱从GEO数据库下载。GSE18606 数据集包含八个 IVIG 抗性 KD 样本和九个适合年龄的健康对照。进行基因本体论（GO）和京都基因与基因组百科全书通路分析，并通过Cytoscape软件构建差异表达基因（DEGs）的蛋白质-蛋白质相互作用（PPI）网络。总共在IVIG抗性KD中鉴定了73个DEG，包括58个上调基因和15个下调基因。GO分析结果表明，DEGs在中性粒细胞脱颗粒、中性粒细胞介导的免疫和参与免疫反应的中性粒细胞活化的生物过程中显着富集。其中选择了10个具有高度连通性的枢纽基因（S100A8、S100A9、S100A12、HGF、LCN2、LY96、CTGF、MMP8、IRAK3和SLPI）。本研究表明，鉴定出的 DEGs 和 hub 基因促进了我们对 IVIG 耐药 KD 发展的分子机制的理解，并可能用作治疗 IVIG 耐药 KD 的分子靶标和诊断生物标志物。选择了具有高度连通性的 S100A9、S100A12、HGF、LCN2、LY96、CTGF、MMP8、IRAK3 和 SLPI)。本研究表明，鉴定出的 DEGs 和 hub 基因促进了我们对 IVIG 耐药 KD 发展的分子机制的理解，并可能用作治疗 IVIG 耐药 KD 的分子靶标和诊断生物标志物。选择了具有高度连通性的 S100A9、S100A12、HGF、LCN2、LY96、CTGF、MMP8、IRAK3 和 SLPI)。本研究表明，鉴定出的 DEGs 和 hub 基因促进了我们对 IVIG 耐药 KD 发展的分子机制的理解，并可能用作治疗 IVIG 耐药 KD 的分子靶标和诊断生物标志物。