Wu Yi, Lee Seok-Woo, Hillman Jeffrey D, Progulske-Fox Ann
Department of Oral Biology, College of Dentistry, University of Florida, Gainesville, Florida 32610, USA.
Infect Immun. 2002 Feb;70(2):928-37. doi: 10.1128/IAI.70.2.928-937.2002.
An in vivo expression technology (IVET) system was designed to identify previously unknown virulence genes of Porphyromonas gingivalis. Fourteen ivi (for in vivo induced) genes that are induced during infection in a mouse abscess model were identified in our study. Of these, seven had homology to genes in the NCBI database, and the rest had no homology to reported DNA sequences. In order to determine virulence-related properties of these genes, three mutant strains, deleted of ivi8 (no homology to genes in the database), ivi10 (homologous to a putative TonB-dependent outer membrane receptor protein), and ivi11 (an immunoreactive 33-kDa antigen PG125 in P. gingivalis), were created. The mutants were tested in a mouse abscess model for alterations in virulence relative to the wild type by a competition assay in BALB/c mice. After 5 days we observed the enrichment of the wild-type strain over mutant strains Deltaivi10 and Deltaivi11, which indicated that mutant strains Deltaivi10 and Deltaivi11 are less able to survive in this model than the wild-type strain, while Deltaivi8 survives as well as the wild-type strain. We propose that knockout of these ivi genes reduced the ability of the mutated P. gingivalis to survive and cause infection compared to the wild-type strain at the site of injection. Also, in separate experiments, groups of mice were challenged with subcutaneous injections of each individual mutant strain (Deltaivi8, Deltaivi10, and Deltaivi11) or with the wild-type strain alone and were then examined to assess their general health status. The results showed that knockout of these ivi genes conferred a reduction in virulence. The ability of the mutants to invade KB cells compared to the wild type was also determined. Interestingly, the CFU counts of the mutant strain Deltaivi10 recovered from KB cells were eight times lower than those of the wild type, indicating that this mutant has a lower capacity for invasion. These results demonstrate that IVET is a powerful tool in discovering virulence genes and the significant role that ivi genes play in the pathogenesis of this species.
设计了一种体内表达技术(IVET)系统来鉴定牙龈卟啉单胞菌先前未知的毒力基因。在我们的研究中,鉴定出了14个在小鼠脓肿模型感染期间被诱导的ivi(体内诱导)基因。其中,7个与NCBI数据库中的基因具有同源性,其余的与已报道的DNA序列无同源性。为了确定这些基因与毒力相关的特性,构建了3个突变株,分别缺失ivi8(与数据库中的基因无同源性)、ivi10(与一种假定的依赖TonB的外膜受体蛋白同源)和ivi11(牙龈卟啉单胞菌中的一种免疫反应性33 kDa抗原PG125)。通过在BALB/c小鼠中进行竞争试验,在小鼠脓肿模型中测试这些突变株相对于野生型的毒力变化。5天后,我们观察到野生型菌株相对于突变株Deltaivi10和Deltaivi11有所富集,这表明突变株Deltaivi10和Deltaivi11在该模型中的存活能力低于野生型菌株,而Deltaivi8的存活能力与野生型菌株相同。我们认为,与野生型菌株相比,敲除这些ivi基因降低了突变牙龈卟啉单胞菌在注射部位存活和引起感染的能力。此外,在单独的实验中,给小鼠皮下注射各个突变株(Deltaivi8、Deltaivi10和Deltaivi11)或单独注射野生型菌株,然后检查以评估它们的总体健康状况。结果表明,敲除这些ivi基因导致毒力降低。还测定了突变株与野生型相比侵袭KB细胞的能力。有趣的是,从KB细胞中回收的突变株Deltaivi10的CFU计数比野生型低8倍,表明该突变株的侵袭能力较低。这些结果表明,IVET是发现毒力基因的有力工具,并且ivi基因在该物种的发病机制中发挥着重要作用。