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Infection and Immunity, February 2002, p. 928-937, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 10.1128/IAI.70.2.928-937.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Identification and Testing of Porphyromonas gingivalis Virulence Genes with a pPGIVET System

Yi Wu, Seok-Woo Lee, Jeffrey D. Hillman, and Ann Progulske-Fox*

Department of Oral Biology, College of Dentistry, University of Florida, Gainesville, Florida 32610

Received 16 July 2001/ Returned for modification 21 August 2001/ Accepted 22 October 2001

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 {Delta}ivi10 and {Delta}ivi11, which indicated that mutant strains {Delta}ivi10 and {Delta}ivi11 are less able to survive in this model than the wild-type strain, while {Delta}ivi8 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 ({Delta}ivi8, {Delta}ivi10, and {Delta}ivi11) 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 {Delta}ivi10 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.

* Corresponding author. Mailing address: Department of Oral Biology, University of Florida, 1600 SW Archer Rd., Rm. DG-45, Gainesville, FL 32610. Phone: (352) 846-0770. Fax: (352) 392-2361. E-mail: apfox{at}dental.ufl.edu.

Editor: D. L. Burns

Infection and Immunity, February 2002, p. 928-937, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 10.1128/IAI.70.2.928-937.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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