Wei Wenqiang, Kong Wanting
School of Basic Medical Sciences, Henan University, Kaifeng, 475004, China.
Department of Physiology and Immunology Programme, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, 117456, Singapore.
Braz J Microbiol. 2019 Jan;50(1):13-22. doi: 10.1007/s42770-018-0021-6. Epub 2018 Dec 17.
Sendai virus (SeV) has been used as a model strain to reveal molecular features of paramyxovirus biology. In this study, we comprehensively analyzed the gene profiling of murine macrophages and airway epithelial cells in response to SeV using gene expression data. The significantly differentially expressed genes (DEGs) were screened by GEO2R. Gene ontology (GO) and pathway enrichment analyses were performed by DAVID. The protein-protein interaction (PPI) map of DEGs was constructed by STRING. The modules of PPI network are produced by molecular complex detection (MCODE) plug-in of Cytoscape. In total, 241 up- and 83 downregulated DEGs were identified in airway epithelial cells while 130 up- and 148 downregulated in macrophage. Particularly, Tmem119 and Colla2 are significantly downregulated in airway epithelial cells and macrophages, respectively. Functional enrichment analysis showed that upregulated DEGs are clustered in innate immunity and inflammatory response in both cell types, whereas downregulated DEGs are involved in host metabolic pathway in airway epithelial cells. PI3K-AKT signaling pathway is downregulated in macrophages. PPI network analysis indicated that some high degree of nodes exist in both cell types, such as Stat1, Tnf, and Cxcl10. In conclusion, SeV infection can induce different host cell responses in airway epithelial cells and macrophages.
仙台病毒(SeV)已被用作揭示副粘病毒生物学分子特征的模型毒株。在本研究中,我们利用基因表达数据全面分析了小鼠巨噬细胞和气道上皮细胞对SeV反应的基因谱。通过GEO2R筛选出显著差异表达基因(DEGs)。利用DAVID进行基因本体(GO)和通路富集分析。通过STRING构建DEGs的蛋白质-蛋白质相互作用(PPI)图谱。PPI网络的模块由Cytoscape的分子复合物检测(MCODE)插件生成。在气道上皮细胞中总共鉴定出241个上调和83个下调的DEGs,而在巨噬细胞中分别为130个上调和148个下调。特别地,Tmem119和Colla2在气道上皮细胞和巨噬细胞中分别显著下调。功能富集分析表明,上调的DEGs在两种细胞类型中均聚集在固有免疫和炎症反应中,而下调的DEGs在气道上皮细胞中参与宿主代谢途径。PI3K-AKT信号通路在巨噬细胞中下调。PPI网络分析表明,两种细胞类型中均存在一些高度节点,如Stat1、Tnf和Cxcl10。总之,SeV感染可诱导气道上皮细胞和巨噬细胞产生不同的宿主细胞反应。