Shea J E, Beuzon C R, Gleeson C, Mundy R, Holden D W
Department of Infectious Diseases, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom.
Infect Immun. 1999 Jan;67(1):213-9. doi: 10.1128/IAI.67.1.213-219.1999.
We have investigated the in vivo growth kinetics of a Salmonella 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.
我们研究了鼠伤寒沙门氏菌菌株(P11D10)的体内生长动力学,该菌株在ssaJ基因中发生了突变,ssaJ是沙门氏菌致病岛2(SPI2)基因,编码小鼠全身生长所需的III型分泌系统的一个组成部分。通过腹腔途径接种后长达8小时,从BALB/c小鼠的脾脏和肝脏中回收的突变型和野生型细胞数量相似。此后,野生型细胞数量在这些器官中继续呈对数增加,而P11D10细胞数量在被清除前的几天内保持相对稳定。对从感染小鼠中回收的脾细胞悬液进行庆大霉素保护实验表明,存活的细胞内野生型细菌随时间积累,但细胞内P11D10细胞没有。还使用携带温度敏感质粒pHSG422的野生型和P11D10细胞进行了感染实验,以区分细菌在体内的生长速率和杀伤情况。接种后16小时,感染小鼠脾脏中的野生型细胞比突变型细胞多10倍,但携带非复制性质粒的两种菌株的细胞数量非常相似,这表明两种菌株受到的杀伤程度差异不大,并且SPI2分泌系统在体内一定是细菌复制而非存活所必需的。小鼠中的SPI2突变表型与携带沙门氏菌毒力质粒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,构建了携带SPI2和spv突变的双突变菌株,并在毒力减弱方面与携带单突变的菌株进行了比较。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。