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A transcriptome analysis focusing on inflammation-related genes of grass carp intestines following infection with Aeromonas hydrophila

机译:侧重于嗜水气单胞菌感染后草鱼肠道炎症相关基因的转录组分析

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摘要

Inflammation is a protective response that is implicated in bacterial enteritis and other fish diseases. The inflammatory mechanisms behind Aeromonas hydrophila infections in fish remain poorly understood. In this study, we performed a de novo grass carp transcriptome assembly using Illumina’s Solexa sequencing technique. On this basis we carried out a comparative analysis of intestinal transcriptomes from A. hydrophila-challenged and physiological saline solution (PSS/mock) -challenged fish, and 315 genes were up-regulated and 234 were down-regulated in the intestines infected with A. hydrophila. The GO enrichment analysis indicated that the differentially expressed genes were enriched to 12, 4, and 8 GO terms in biological process, molecular function, and cellular component, respectively. A KEGG analysis showed that 549 DEGs were involved in 165 pathways. Moreover, 15 DEGs were selected for quantitative real-time PCR analysis to validate the RNA-seq data. The results confirmed the consistency of the expression levels between RNA-seq and qPCR data. In addition, a time-course analysis of the mRNA expression of 12 inflammatory genes further demonstrated that the intestinal inflammatory responses to A. hydrophila infection simultaneously modulated gene expression variations. The present study provides intestine-specific transcriptome data, allowing us to unravel the mechanisms of intestinal inflammation triggered by bacterial pathogens.
机译:炎症是一种保护性反应,与细菌性肠炎和其他鱼类疾病有关。鱼类中嗜水气单胞菌感染背后的炎症机制仍知之甚少。在这项研究中,我们使用Illumina的Solexa测序技术进行了从头开始的草鱼转录组组装。在此基础上,我们对嗜水链球菌和生理盐溶液(PSS /模拟)攻击的鱼类的肠道转录组进行了比较分析,并在受A感染的肠道中上调了315个基因,下调了234个基因。亲水性GO富集分析表明差异表达的基因分别在生物学过程,分子功能和细胞成分方面富集到12、4和8个GO项。 KEGG分析表明,有549个DEG参与了165个途径。此外,选择了15个DEG用于实时定量PCR分析以验证RNA-seq数据。结果证实了RNA-seq和qPCR数据之间表达水平的一致性。另外,对12种炎性基因的mRNA表达进行时程分析进一步证明,对嗜水链球菌感染的肠道炎性反应同时调节基因表达变异。本研究提供了肠道特异性转录组数据,使我们能够揭示由细菌病原体引发的肠道炎症的机制。

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