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2型丝氨酸/苏氨酸磷酸酶1是一种重要的毒力因子。

A serine/threonine phosphatase 1 of type 2 is an important virulence factor.

作者信息

Fang Lihua, Zhou Jingjing, Fan Pengcheng, Yang Yunkai, Shen Hongxia, Fang Weihuan

机构信息

Zhejiang University Institute of Preventive Veterinary Medicine and Zhejiang Provincial Key Laboratory of Preventive Veterinary Medicine, Hangzhou 310058, China.

Center for Synthetic Biology Engineering Research, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, China.

出版信息

J Vet Sci. 2017 Dec 31;18(4):439-447. doi: 10.4142/jvs.2017.18.4.439.

Abstract

is regarded as one of the major pathogens of pigs, and type 2 (SS2) is considered a zoonotic bacterium based on its ability to cause meningitis and streptococcal toxic shock-like syndrome in humans. Many bacterial species contain genes encoding serine/threonine protein phosphatases (STPs) responsible for dephosphorylation of their substrates in a single reaction step. This study investigated the role of in the pathogenesis of SS2. An isogenic mutant (Δ) was constructed from SS2 strain ZJ081101. The Δ mutant exhibited a significant increase in adhesion to HEp-2 and bEnd.3 cells as well as increased survival in RAW264.7 cells, as compared to the parent strain. Increased survival in macrophage cells might be related to resistance to reactive oxygen species since the Δ mutant was more resistant than its parent strain to paraquat-induced oxidative stress. However, compared to parent strain virulence, deletion of significantly attenuated virulence of SS2 in mice, as shown by the nearly double lethal dose 50 value and the lower bacterial load in organs and blood in the murine model. We conclude that Stp1 has an essential role in SS2 virulence.

摘要

被认为是猪的主要病原体之一,而2型(SS2)因其能够在人类中引起脑膜炎和链球菌中毒性休克样综合征而被视为一种人畜共患病细菌。许多细菌物种含有编码丝氨酸/苏氨酸蛋白磷酸酶(STP)的基因,这些基因负责在单一反应步骤中使其底物去磷酸化。本研究调查了[具体基因名称未给出]在SS2发病机制中的作用。从SS2菌株ZJ081101构建了一个同基因[具体基因名称未给出]突变体(Δ[具体基因名称未给出])。与亲本菌株相比,Δ[具体基因名称未给出]突变体对HEp-2和bEnd.3细胞的黏附显著增加,并且在RAW264.7细胞中的存活率也增加。巨噬细胞中存活率的增加可能与对活性氧的抗性有关,因为Δ[具体基因名称未给出]突变体比其亲本菌株对百草枯诱导的氧化应激更具抗性。然而,与亲本菌株的毒力相比,[具体基因名称未给出]的缺失显著减弱了SS2在小鼠中的毒力,如在小鼠模型中致死剂量50值几乎翻倍以及器官和血液中的细菌载量较低所示。我们得出结论,Stp1在SS2毒力中起重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f535/5746436/0030ec13b11b/jvs-18-439-g001.jpg

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