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鉴定猪链球菌 2 型在天然宿主中特异性表达的基因。

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

机构信息

Division of Animal Infectious Diseases in the State Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Shizishan Street 1, Hongshan District, Wuhan, Hubei 430070, China.

出版信息

Int J Med Microbiol. 2010 Nov;300(7):482-8. doi: 10.1016/j.ijmm.2010.04.018. Epub 2010 May 31.

Abstract

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.

摘要

猪链球菌 2 型(SS2)是一种重要的猪源和人源动物致病菌。先前关于 SS2 感染机制的研究主要建立在体外或离体模型上。在本研究中,我们专注于鉴定 SS2 在自然感染猪体内的体内优先表达基因。通过选择性捕获转录序列(SCOTS)和比较点印迹分析,鉴定了 80 个在猪脑和肺中上调的 SS2 基因,随后通过定量 RT-PCR 验证。这些基因可分为 5 个功能类别:代谢、细胞壁相关蛋白、转运蛋白、细胞复制和功能未知。其中一些基因可能通过以下策略有助于 SS2 在宿主中的存活和发病机制。首先,SS2 通过改变其代谢和细胞壁组成来逃避宿主先天免疫清除,分别由相应基因 ldh 和 pbp2A 的上调表明。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,该系统可能作用于目标基因,如参与应激反应和细胞壁生物合成的 pcsB。第三,SS2 通过上调毒力基因,如 sly、pdgA、ssp、gidA、gcp 和 hp1311,增强其体内毒力。进一步研究这些体内上调的基因将有助于了解 SS2 的体内生存机制和发病机制。

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