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Porphyromonas gingivalis htrA is involved in cellular invasion and in vivo survival

Lihui Yuan^1,,

Paulo H. Rodrigues^1,

¹ Department of Oral Biology, College of Dentistry and Center for Molecular Microbiology, University of Florida, Gainesville, FL 32610, USA
² Department of Anatomy and Cell Biology, College of Medicine and Center for Molecular Microbiology, University of Florida, Gainesville, FL 32610, USA

Correspondence
Ann Progulske-Fox
apfox{at}dental.ufl.edu

HtrA is a heat-stress protein that functions both as a chaperone and as a serine protease. HtrA has been shown in several organisms to be involved in responses to stressful environmental conditions and involvement of HtrA in virulence has been reported in pathogenic species. A Porphyromonas gingivalis htrA mutant demonstrated no significant difference to the W83 parent strain when subjected to high temperature and pH values from 3 to 11. However, the htrA mutant showed increased sensitivity to H₂O₂. Cell invasion assays indicated that the total interaction (adherence) with KB cells, human coronary artery endothelial cells and gingival epithelial cells (GEC) was the same for both the wild-type and the htrA mutant. However, the htrA mutant showed increased invasion in KB cells and GEC. Microarray experiments indicated that a total of 253 genes were differentially regulated in the htrA mutant, including a group of stress-related genes, which might be responsible for the observed decreased resistance to H₂O₂. In animal experiments, a competition assay showed that the htrA mutant did not survive as well as the wild-type. In another in vivo assay, fewer mice infected with the htrA mutant died than mice infected with W83, suggesting that the htrA gene is virulence-related. These data indicate that the htrA gene in P. gingivalis does not relate to stress conditions such as high temperature and pH, but rather to H₂O₂ stress. The htrA gene also appears to be important for virulence and survival in in vivo animal models.

These authors contributed equally to this work.

Present address: Department of Physiology, College of Medicine, University of Florida, Gainesville, FL 32610, USA.

The GEO accession number for the microarray data reported in this paper is GSE10027.