猪圆环病毒
生物
蛋白质组
蛋白质组学
无标记量化
免疫系统
实时聚合酶链反应
污渍
串联质量标签
定量蛋白质组学
分子生物学
细胞生物学
基因
免疫学
病毒
生物信息学
遗传学
作者
Haijun Jiang,Wei Li,Dan Wang,Jing Wang,Shanshan Zhu,Ruiping She,Tianlong Liu,Jijing Tian,Rong Quan,Lei Hou,Zixuan Li,Jun Chu,Jiyong Zhou,Yuxin Guo,Yanyang Xi,Huiqi Song,Yuan Feng,Jue Liu
标识
DOI:10.1016/j.jprot.2019.103598
摘要
Porcine circovirus type 3 (PCV3) infection induces porcine dermatitis and nephropathy syndrome, reproductive failure, and multisystemic inflammatory lesions in piglets and sows. To better understand the host responses to PCV3 infection, isobaric tags for relative and absolute quantification (iTRAQ) labeling combined with LC-MS/MS analysis was used for quantitative determination of differentially regulated cellular proteins in the lungs of specific-pathogen-free piglets after 4 weeks of PCV3 infection. Totally, 3429 proteins were detected in three independent mass spectrometry analyses, of which 242 differential cellular proteins were significantly regulated, consisting of 100 upregulated proteins and 142 downregulated proteins in PCV3-infected group relative to control group. Bioinformatics analysis revealed that these higher or lower abundant proteins involved primarily metabolic processes, innate immune response, MHC-I and MHC-II components, and phagosome pathways. Ten genes encoding differentially regulated proteins were selected for investigation via real-time RT-PCR. The expression levels of six representative proteins, OAS1, Mx1, ISG15, IFIT3, SOD2, and HSP60, were further confirmed by Western blotting and immunohistochemistry. This study attempted for the first time to investigate the protein profile of PCV3-infected piglets using iTRAQ technology; our findings provide valuable information to better understand the mechanisms underlying the host responses to PCV3 infection in piglets. SIGNIFICANCE: Our study identified differentially abundant proteins related to a variety of potential signaling pathways in the lungs of PCV3-infected piglets. These findings provide valuable information to better understand the mechanisms of host responses to PCV3 infection.
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