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Identification of Streptococcus suis serotype 2 genes preferentially expressed in the natural host

机译:在自然宿主中优先表达的猪链球菌血清型2基因的鉴定

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摘要

Streptococcus suis serotype 2 (SS2) is an important zoonotic pathogen for swine and humans. Previous research about the mechanism of SS2 infection was largely established on in vitro or ex vivo models. In this study, we focused on the identification of SS2 genes preferentially expressed in vivo during natural infection in pigs. Eighty SS2 genes were identified to be up-regulated in the porcine brains and lungs by selective capture of transcribed sequences (SCOTS) and comparative dot blot analysis, followed by quantitative RT-PCR validation. These genes could be classified into 5 functional categories: metabolism, cell wall associated proteins, transporters, cell replication, and function unknown. Some of these genes may contribute to the survival and pathogenesis of SS2 in the host via the following strategies. First, SS2 evades the host innate immune clearance through modifying its metabolism and cell wall composition as indicated by the up-regulation of the corresponding gene ldh and pbp2A, respectively. Secondly, SS2 adapts to the in vivo conditions by inducing the expression of the two-component signal transduction system VicKR which may function on the target genes such as pcsB involved in stress response and cell wall biosynthesis. Thirdly, SS2 enhances its virulence in vivo by up-regulating the virulence genes, such as sly, pdgA, ssp, gidA, gcp and hp1311. Further study of these in vivo up-regulated genes will contribute to understanding the in vivo survival mechanism and pathogenesis of SS2.
机译:猪链球菌血清型2(SS2)是猪和人的重要人畜共患病原体。关于SS2感染机制的先前研究主要建立在体外或离体模型上。在这项研究中,我们专注于鉴定猪自然感染期间体内优先表达的SS2基因。通过选择性捕获转录序列(SCOTS)和比较斑点印迹分析,然后通过定量RT-PCR验证,鉴定出80种SS2基因在猪脑和肺中被上调。这些基因可以分为5个功能类别:新陈代谢,细胞壁相关蛋白,转运蛋白,细胞复制和未知功能。这些基因中的某些可能通过以下策略有助于宿主中SS2的存活和发病机理。首先,SS2通过修饰其代谢和细胞壁组成来逃避宿主的先天免疫清除,这分别由相应基因ldh和pbp2A的上调指示。其次,SS2通过诱导双组分信号转导系统VicKR的表达来适应体内条件,该系统可能对参与应激反应和细胞壁生物合成的目标基因(例如pcsB)起作用。第三,SS2通过上调毒力基因,例如sly,pdgA,ssp,gidA,gcp和hp1311来增强其体内毒力。这些体内上调基因的进一步研究将有助于了解SS2的体内存活机制和发病机理。

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