Large-scale profiling of the proteome and dual transcriptome in Nile tilapia (Oreochromis niloticus) challenged with low- and high-virulence strains of Streptococcus agalactiae
Large-scale profiling of the proteome and dual transcriptome in Nile tilapia (Oreochromis niloticus) challenged with low- and high-virulence strains of Streptococcus agalactiae
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对受到低毒力和高毒力无乳链球菌菌株攻击的尼罗罗非鱼（Oreochromis niloticus）的蛋白质组和双转录组进行大规模分析
DOI：
10.1016/j.fsi.2020.03.008
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发表时间：
2020
影响因子：
4.7
通讯作者：
Chen Ming
中科院分区：
文献类型：
--
作者：
Zhou Yi;Liu Yu;Luo Yongju;Zhong Huan;Huang Ting;Liang Wanwen;Xiao Jun;Wu Wende;Li Liping;Chen Ming
无乳链球菌是水产动物特别是罗非鱼的常见病原菌，严重影响水产养殖业的发展，造成严重的经济损失。此前，从感染的罗非鱼中分离到一株无乳杆菌HN 016，经胰蛋白酶大豆肉汤（TSB）连续传代，获得一株弱毒株YM 001。YM001已被证明是一种安全的S.罗非鱼无乳感染。为了了解这两种菌株毒力的分子基础，我们进行了蛋白质组学和转录组学分析，以揭示在感染过程中肝脏和肠道中蛋白质和基因表达的变化。HN 016显著降低了白色细胞（WBC）、中性粒细胞（NEU）、红细胞（RBC）和红细胞压积（HCT）的含量，提高了总蛋白（TP）、白蛋白（ALB）和球蛋白（GLO）的含量，而对照组与YM 001组相比差异不显著。在感染过程中，致病性肽聚糖水解酶、CSPA和膜蛋白在YM001和HN 016之间存在显著差异表达。此外，蛋白质组和转录组数据均显示，与HN 016感染相比，YM001感染分别刺激了肝脏和肠道中的补体和凝血级联途径以及抗原加工和呈递途径。对病原菌关键毒力基因的互作网络分析表明，CSPA作为关键节点，影响DOLPP 1、MIPEP、PA2G4、OCIAD 1、G3BP 1和CLIC 5的表达，且呈正相关。目前的证据表明，在感染过程中，CSPA基因是导致YM001低致病力的关键基因。
Streptococcus agalactiae is a common pathogen in aquatic animals, especially tilapia, that hinders aquaculture development and leads to serious economic losses. Previously, aS. agalactiaestrain named HN016 was identified from infected tilapia, and the attenuated strain YM001 was subsequently obtained by continuous passaging in Tryptic Soy Broth (TSB) medium. YM001 has been demonstrated as a safe vaccine forS. agalactiaeinfection in tilapia. To understand the molecular bases of the virulence of these two strains, we performed proteomic and transcriptomic analysis to reveal the protein and gene expression changes in the liver and intestine during the infection process. HN016 significantly decreased the contents of white blood cells (WBCs), neutrophils (NEUs), red blood cells (RBCs) and hematocrit (HCT) and increased the levels of total protein (TP), albumin (ALB) and globulin (GLO), while no such significant differences were observed when comparing the control with YM001. During the infection process, pathogenic peptidoglycan hydrolase, CSPA and membrane proteins were significantly differentially expressed between YM001 and HN016. Furthermore, both proteome and transcriptome data showed that the complement and coagulation cascades pathway and the antigen processing and presentation pathway were stimulated in the liver and intestine, respectively, by YM001 infection compared to HN016 infection. The interaction network analysis of key virulence genes from pathogens suggested that CSPA, as a key node, affects the expression of DOLPP1, MIPEP, PA2G4, OCIAD1, G3BP1 and CLIC5 with a positive correlation. The present evidence suggests that during the infection process, CSPA was the key genes contributing to low virulence in YM001.