Comparative transcriptome analysis reveals induction of apoptosis in chicken kidney cells associated with the virulence of nephropathogenic infectious bronchitis virus.
Comparative transcriptome analysis reveals induction of apoptosis in chicken kidney cells associated with the virulence of nephropathogenic infectious bronchitis virus.
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比较转录组分析揭示鸡肾细胞凋亡的诱导与肾病性传染性支气管炎病毒的毒力相关
DOI：
10.1016/j.micpath.2017.11.031
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发表时间：
2017-12
影响因子：
3.8
通讯作者：
Wang H
中科院分区：
文献类型：
--
作者：
Liu H;Yang X;Zhang Z;Li J;Zou W;Zeng F;Wang H
鸡传染性支气管炎病毒（Avian Infectious Bronchitis Virus，IBV）是引起鸡呼吸道和肾脏疾病的主要病原，在世界范围内造成严重的经济损失。肾致病性IBV毒株本质上引起肾炎和肾脏病变，其致病机制尚不清楚。本研究用3种不同毒力的肾型IBV感染SPF鸡，在转录组水平上比较了它们在鸡肾脏中的基因表达谱。结果表明，与假感染组相比，SCDY 2强毒接种组、SCK 2强毒接种组和LDT 3-A非强毒接种组分别有1279个、145个和74个差异表达基因。GO和KEGG途径富集分析显示，上调表达的DE基因主要参与细胞凋亡，下调表达的DE基因主要参与代谢过程和DNA复制。蛋白质相互作用（PPI）分析表明，SCDY 2组DE基因形成了一个网络，网络的核心是细胞凋亡蛋白和免疫应答蛋白。基因表达谱的聚类分析表明，SCDY 2强毒组中上调的DE基因在SCK 2强毒组中均有不同程度的上调，而SCDY 2弱毒组中下调的DE基因在SCK 2强毒组中也有不同程度的下调。此外，实验检测到的肾组织凋亡细胞数在3个病毒接种组间差异很大，且与病毒滴度、肾脏病变程度和病毒毒力呈正相关。综上所述，本研究表明，强毒肾致病性IBV感染改变了许多基因表达，诱导肾细胞凋亡可能是强毒肾致病性IBV的主要致病决定因素。采用转录组分析方法研究了3种肾型IBV感染后鸡肾细胞基因表达的变化。攻击后DE基因主要参与细胞凋亡、免疫应答、代谢和DNA复制等途径。细胞凋亡的激活和天然免疫应答的抑制与IBV的毒力相一致。细胞凋亡的诱导是由感染后免疫应答的抑制和病毒的生产性复制触发的。
Avian infectious bronchitis virus (IBV) that causes respiratory and nephritic diseases in chicken is a major poultry pathogen leading to serious economic loss worldwide. The nephropathogenic IBV strains cause nephritis and kidney lesions intrinsically and the pathogenic mechanism is still unclear. In the present study, SPF chicks were infected with three nephropathogenic IBVs of different virulence and their gene expression profiles in chicken kidney were compared at transcriptome level. As a result, 1279 differentially expressed (DE) genes were found in very virulent SCDY2 inoculated group, 145 in virulent SCK2 group and 74 in non-virulent LDT3-A group when compared to mock infected group. Gene Ontology (GO) and KEGG pathway enrichment analysis on SCDY2 group displayed that the up-regulated DE genes were mainly involved in cell apoptosis, and the down-regulated genes were involved in metabolic processes and DNA replication. Protein-Protein Interaction (PPI) analysis showed that DE genes in SCDY2 group formed a network, and the core of the network was composed by cell apoptosis and immune response proteins. The clustering of gene expression profile among the three virus inoculated groups indicated that the majority of up-regulated DE genes on apoptosis in very virulent SCDY2 group were up-regulated more or less in virulent SCK2 group and those down-regulated on innate immune response in SCDY2 group were also down-regulated differently in SCK2 group. In addition, the number of apoptotic cells detected experimentally in kidney tissue were very different among the three virus inoculated groups and were positively accordant with the viral titer, kidney lesions and viral virulence of each group. Taken all together, the present study revealed that virulent nephropathogenic IBV infection modified a number of gene expression and induction of apoptosis in kidney cells may be a major pathogenic determinant for virulent nephropathogenic IBV. Genes expression in chicken kidney cells post inoculation of three nephro IBVs was studied by transcriptome analysis. DE genes post challenge mainly involved in the pathways of apoptosis, immune response, metabolic and DNA replication. Activation of apoptosis and suppression of innate immune response were accordant with the virulence of inoculated IBVs. Induction of apoptosis is triggered by suppression of immune response and productive replication of virus post infection.
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