罗非鱼感染无乳链球菌前后血浆蛋白组学的差异表达分析

Differential expression analysis of plasma proteomics in Nile tilapia(GIFT)before and after infection with Streptococcus agalactiae

为了探究罗非鱼(Oreochromis spp.)感染无乳链球菌(Streptococcus agalactiae)前后血浆蛋白的差异表达及其相关的信号通路,选取体质健康、规格统一的吉富罗非鱼(Oreochromis niloticus GIFT,体质量为150 g±10 g)86尾,随机分成两组,试验组鱼体腹腔注射浓度为5×10^(7)CFU/mL的无乳链球菌WC1535菌液100μL,对照组鱼体腹腔注射无菌PBS溶液100μL,攻毒6 h后,采集两组罗非鱼的血浆,利用蛋白组学技术分析罗非鱼感染无乳链球菌前后的血浆差异表达蛋白,并分别对差异表达蛋白进行GO和KEGG富集分析。结果表明:罗非鱼感染无乳链球菌前后共鉴定出751个蛋白,其中显著差异蛋白34个,包括9个显著上调,25个显著下调;GO功能注释显示,这些差异蛋白主要与结合、运动、催化等功能有关;KEGG富集通路分析显示,差异蛋白在肌动蛋白细胞骨架调节、MAPK信号通路、癌症中心碳代谢和癌症相关蛋白聚糖等通路显著富集。研究表明,罗非鱼感染无乳链球菌前后,其血浆差异蛋白主要富集于鱼体能量代谢、细胞运动和免疫调节等相关的信号通路,该结果为进一步研究罗非鱼感染无乳链球菌的相关分子机制提供了基础数据。

In order to probe the differentially expressed proteins(DEPs)of plasma and their associated signaling pathways from Nile tilapia(GIFT)Oreochromis niloticus before and after infection with Streptococcus agalactiae,the plasma DEPs were analyzed in the plasma collected from the tilapia with body weight of(150 g±10 g)intraperitoneally injected with 100μL of S.agalactiae WC1535 suspension at concentration of 5×10^(7)CFU/mL in the experimental group and 100μL sterile PBS in the control group in via proteomics after 6 h of challenge via proteomics.Furthermore,GO and KEGG enrichment was performed for the DEPs.The results showed that 751 proteins were identified in the tilapia plasma,with 34 significantly different proteins including 9 proteins significantly up-regulated and 25 proteins significantly down-regulated.GO functional annotation showed that these DEPs were mainly involved in binding,motility and catalysis functions.KEGG pathway enrichment analysis revealed that the DEPs were significantly enriched in regulation of actin cytoskeleton,MAPK signaling pathway,central carbon metabolism in cancer,and proteoglycans in cancer.It was found that the DEPs from the tilapia infected with S.agalactiae were mainly enriched in the pathways related to energy metabolism,cellular motility and immune regulation.The findings provided basic data for further research on the molecular mechanisms of S.agalactiae infection in tilapia.