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首页> 外文期刊>Infection and immunity >Influence of the Salmonella typhimuriumPathogenicity Island 2 Type III Secretion System on Bacterial Growth in the Mouse
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Influence of the Salmonella typhimuriumPathogenicity Island 2 Type III Secretion System on Bacterial Growth in the Mouse

机译：鼠伤寒沙门氏菌致病岛2 III型分泌系统对小鼠细菌生长的影响

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We have investigated the in vivo growth kinetics of aSalmonella typhimurium strain (P11D10) carrying a mutation in ssaJ, a Salmonella pathogenicity island 2 (SPI2) gene encoding a component of a type III secretion system required for systemic growth in mice. Similar numbers of mutant and wild-type cells were recovered from the spleens and livers of BALB/c mice up to 8 h after inoculation by the intraperitoneal route. Thereafter, the numbers of wild-type cells continued to increase logarithmically in these organs, whereas those of P11D10 remained relatively static for several days before being cleared. Gentamicin protection experiments on spleen cell suspensions recovered from infected mice showed that viable intracellular wild-type bacteria accumulated over time but that intracellular P11D10 cells did not. Infection experiments were also performed with wild-type and P11D10 cells carrying the temperature-sensitive plasmid pHSG422 to distinguish between bacterial growth rates and killing in vivo. At 16 h postinoculation there were 10-fold more wild-type cells than mutant cells in the spleens of infected mice, but the numbers of cells of both strains carrying the nonreplicating plasmid were very similar, showing that there was little difference in the degree of killing sustained by the two strains and that the SPI2 secretion system must be required for bacterial replication, rather than survival, in vivo. The SPI2 mutant phenotype in mice is similar to that of strains carrying mutations in the Salmonella virulence plasmid spv genes. To determine if these two sets of genes interact together, a double mutant strain carrying SPI2 and spv mutations was constructed and compared with strains carrying single mutations in terms of virulence attenuation. These experiments failed to provide any evidence showing that the SPI2 and spv gene products interact together as part of the same virulence mechanism.
机译：我们已经研究了携带 ssaJ （一个 Salmonella 致病岛2（SPI2）的一个突变体的鼠伤寒沙门氏菌（P11D10）的体内生长动力学）编码小鼠全身生长所需的III型分泌系统成分的基因。通过腹膜内途径接种后直至8小时，从BALB / c小鼠的脾脏和肝脏中回收到相似数量的突变和野生型细胞。此后，这些器官中野生型细胞的数量继续呈对数增长，而P11D10的数量在清除前仍保持相对静止。庆大霉素对从感染小鼠中回收的脾细胞悬液的保护实验表明，存活的细胞内野生型细菌会随时间积累，而细胞内的P11D10细胞则不会。还对携带温度敏感质粒pHSG422的野生型和P11D10细胞进行了感染实验，以区分细菌的生长速率和体内杀伤作用。接种后16 h，感染小鼠脾脏中的野生型细胞比突变型细胞多10倍，但是两种携带非复制质粒的菌株的细胞数量非常相似，表明二者的程度差异不大。这两种菌株都具有致命的杀伤力，并且必须要在体内细菌复制而不是生存需要SPI2分泌系统。小鼠中的SPI2突变表型与携带 Salmonella 毒力质粒 spv 基因突变的菌株相似。为了确定这两组基因是否相互作用，构建了一个带有SPI2和 spv 突变的双突变株，并将其与单个突变的毒力衰减比较。这些实验未能提供任何证据表明SPI2和 spv 基因产物作为同一毒力机制的一部分相互作用。

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