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3
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Genome-wide Analysis of Salmonella enterica serovar Typhi in Humanized Mice Reveals Key Virulence Features.全基因组分析人类源化小鼠中的伤寒沙门氏菌血清型 Typhi 揭示关键毒力特征。
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Growth inhibition of cytosolic Salmonella by caspase-1 and caspase-11 precedes host cell death.细胞质沙门氏菌的生长抑制由胱天蛋白酶-1 和胱天蛋白酶-11 引起,早于宿主细胞死亡。
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伤寒 SPI-2 注入装置之谜。

The Typhi SPI-2 injectisome enigma.

机构信息

Department of Infectious Disease, Centre for Bacterial Resistance Biology, Imperial College London, London, SW7 2AZ, UK.

出版信息

Microbiology (Reading). 2023 Oct;169(10). doi: 10.1099/mic.0.001405.

DOI:10.1099/mic.0.001405
PMID:37862087
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10634361/
Abstract

The pathogenicity island 2 (SPI-2)-encoded type III secretion system (injectisome) is assembled following uptake of bacteria into vacuoles in mammalian cells. The injectisome translocates virulence proteins (effectors) into infected cells. Numerous studies have established the requirement for a functional SPI-2 injectisome for growth of Typhimurium in mouse macrophages, but the results of similar studies involving Typhi and human-derived macrophages are not consistent. It is important to clarify the functions of the . Typhi SPI-2 injectisome, not least because an inactivated SPI-2 injectisome forms the basis for live attenuated . Typhi vaccines that have undergone extensive trials in humans. Intracellular expression of injectisome genes and effector delivery take longer in the . Typhi/human macrophage model than for . Typhimurium and we propose that this could explain the conflicting results. Furthermore, strains of both . Typhimurium and . Typhi contain intact genes for several 'core' effectors. In . Typhimurium these cooperate to regulate the vacuole membrane and contribute to intracellular bacterial replication; similar functions are therefore likely in . Typhi.

摘要

SPI-2 编码的 III 型分泌系统(注入器)在细菌被摄取到哺乳动物细胞的空泡中后组装。注入器将毒力蛋白(效应子)转运到受感染的细胞中。许多研究已经证实,功能性 SPI-2 注入器对于鼠巨噬细胞中鼠伤寒沙门氏菌的生长是必需的,但涉及伤寒沙门氏菌和人源巨噬细胞的类似研究结果并不一致。澄清伤寒沙门氏菌 SPI-2 注入器的功能非常重要,尤其是因为失活的 SPI-2 注入器是经过广泛人体试验的减毒伤寒沙门氏菌疫苗的基础。注入器基因的细胞内表达和效应物的输送在伤寒沙门氏菌/人源巨噬细胞模型中比鼠伤寒沙门氏菌需要更长的时间,我们提出这可以解释矛盾的结果。此外,鼠伤寒沙门氏菌和伤寒沙门氏菌的菌株都含有几个“核心”效应物的完整基因。在鼠伤寒沙门氏菌中,这些基因协同作用来调节空泡膜,并有助于细胞内细菌复制;因此,在伤寒沙门氏菌中可能具有类似的功能。