纳尔逊海湾病毒感染小鼠巨噬细胞RAW264.7的转录物组分析  

Transcriptome analysis of murine RAW264.7 macrophages infected with Nelson Bay virus

作　　者：马竹萍 陈淼娟 孙绿茵 付纹瑞 田晶 李永刚 陶晓莉 MA Zhuping;CHEN Miaojuan;SUN Lüyin;FU Wenrui;TIAN Jing;LI Yonggang;TAO Xiaoli(Department of Pathogen Biology,School of Basic Medicine,Jinzhou Medical University,Jinzhou 121001,China;Department of Cardiology,General Technology Panjin Liaoyou Petroflower Hospital,Panjin 124000,China;Collaborative Innovation Center for Prevention and Control of Zoonoses,Jinzhou Medical University,Jinzhou 121001,China)

机构地区：[1]锦州医科大学基础医学院病原生物学教研室,辽宁锦州121001 [2]通用技术辽油宝石花医院心内科,辽宁盘锦124000 [3]锦州医科大学人畜共患病防控协同创新中心,辽宁锦州121001

出　　处：《中国医科大学学报》2025年第4期340-345,共6页Journal of China Medical University

基　　金：辽宁省科学技术计划(2022-BS-320);辽宁省教育厅高校基本科研项目(24100200014)。

摘　　要：目的通过分析纳尔逊海湾病毒(NBV)感染小鼠巨噬细胞RAW264.7转录物组测序结果,筛选差异表达基因,探讨固有免疫应答在呼肠孤病毒感染中的作用机制。方法用感染复数为30的NBV-Miyazaki病毒株感染小鼠巨噬细胞RAW264.7,运用高通量转录物组测序技术,以q<0.05且|log2FC|≥1为条件,筛选感染组和对照组的差异表达基因,利用基因本体论(GO)和京都基因和基因组数据库(KEGG)对差异表达基因进行富集分析。结果与对照组相比,感染组差异表达的基因共442个,其中显著上调的基因381个,显著下调的基因61个。差异表达基因在GO富集中主要与固有免疫反应、对病毒的防御反应、细胞因子的产生以及细胞对细胞因子刺激的反应等功能相关,在KEGG中主要富集到Toll样受体信号通路、维甲酸诱导基因Ⅰ样受体信号通路、PI3K/Akt等信号通路。结论RAW264.7细胞被NBV-Miyazaki病毒感染后,可以通过激活模式识别受体,促进细胞因子、趋化因子和其他免疫相关因子释放,增强抗体依赖细胞介导的细胞毒作用,以发挥免疫效应,为探究固有免疫在NBV-Miyazaki病毒感染过程中的作用机制提供了理论依据。Objective To analyze the transcriptome sequencing results of Nelson Bay virus(NBV)-infected murine RAW264.7 macrophages,and to screen for differentially expressed genes(DEGs)to provide a theoretical basis for exploring the mechanism of innate immune response in reovirus infection.Methods RAW264.7 cells were infected with the NBV-Miyazaki virus strain at a multiplicity of infection(MOI)of 30.We used transcriptome sequencing technologies,with q<0.05 and|log2FC|≥1,for screening the DEGs in the infection and control groups.The Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)databases were used for enrichment analysis of DEGs.Results A total of 442 genes were differentially expressed in the infection group,of which 381 genes were significantly upregulated and 61 genes were significantly downregulated.In the GO analysis,the enrichment of DEGs was primarily related to the innate immune response,defense response to viruses,cytokine production,and cell response to cytokine stimulation.In the KEGG analysis,the enrichment of DEGs were primarily related to the Toll-like receptor,retinoid acid inducible geneⅠ-like receptor,PI3K/Akt,and other signaling pathways.Conclusion RAW264.7 macrophages infected with the NBV-Miyazaki virus can activate pattern recognition receptors;promote the release of cytokines,chemokines,and other immune-related factors;and enhance antibody-dependent cell-mediated cytotoxicity to exert an immune effect.This study provides a theoretical basis for exploring the mechanisms of innate immunity during NBV-Miyazaki virus infection.

关 键 词：纳尔逊海湾病毒 巨噬细胞 转录物组 

分 类 号：R373.1[医药卫生—病原生物学]