首页> 外文OA文献 >Virulence Plasmid-Borne spvB and spvC Genes Can Replace the 90-Kilobase Plasmid in Conferring Virulence to Salmonella enterica Serovar Typhimurium in Subcutaneously Inoculated Mice
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Virulence Plasmid-Borne spvB and spvC Genes Can Replace the 90-Kilobase Plasmid in Conferring Virulence to Salmonella enterica Serovar Typhimurium in Subcutaneously Inoculated Mice

机译:致病性质粒-Borne spvB和spvC基因可替代90-Kilobase质粒,赋予皮下接种小鼠肠炎沙门氏菌血清型鼠伤寒病毒致病性。

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摘要

In a mouse model of systemic infection, the spv genes carried on the Salmonella enterica serovar Typhimurium virulence plasmid increase the replication rate of salmonellae in host cells of the reticuloendothelial system, most likely within macrophages. A nonpolar deletion in the spvB gene greatly decreased virulence but could not be complemented by spvB alone. However, a low-copy-number plasmid expressing spvBC from a constitutive lacUV5 promoter did complement the spvB deletion. By examining a series of spv mutations and cloned spv sequences, we deduced that spvB and spvC could be sufficient to confer plasmid-mediated virulence to S. enterica serovar Typhimurium. The spvBC-bearing plasmid was capable of replacing all of the spv genes, as well as the entire virulence plasmid, of serovar Typhimurium for causing systemic infection in BALB/c mice after subcutaneous, but not oral, inoculation. A point mutation in the spvBC plasmid preventing translation but not transcription of spvC eliminated the ability of the plasmid to confer virulence. Therefore, it appears that both spvB and spvC encode the principal effector factors for Spv- and plasmid-mediated virulence of serovar Typhimurium.
机译:在全身感染的小鼠模型中,携带肠炎沙门氏菌鼠伤寒沙门氏菌毒力质粒的spv基因增加了网状内皮系统宿主细胞中沙门氏菌的复制率,这很可能是在巨噬细胞内。 spvB基因的非极性缺失大大降低了毒力,但不能单独由spvB补充。但是,从组成型lacUV5启动子表达spvBC的低拷贝数质粒确实补充了spvB缺失。通过检查一系列的spv突变和克隆的spv序列,我们推论spvB和spvC可能足以赋予质粒介导的毒力肠球菌血清鼠伤寒。携带spvBC的质粒能够替换鼠伤寒血清的所有spv基因以及整个毒力质粒,以引起皮下但非口服接种后BALB / c小鼠的全身感染。 spvBC质粒中的点突变阻止了spvC的翻译但不能阻止其转录,从而消除了该质粒赋予毒力的能力。因此,看来spvB和spvC都编码鼠伤寒沙门氏菌的Spv和质粒介导的毒力的主要效应因子。

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