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Infection and Immunity, March 2009, p. 1246-1261, Vol. 77, No. 3
0019-9567/09/$08.00+0     doi:10.1128/IAI.01038-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Porphyromonas gingivalis RgpA-Kgp Proteinase-Adhesin Complexes Penetrate Gingival Tissue and Induce Proinflammatory Cytokines or Apoptosis in a Concentration-Dependent Manner{triangledown}

Neil M. O'Brien-Simpson,{dagger} Rishi D. Pathirana,{dagger} Glenn D. Walker,{dagger} and Eric C. Reynolds*

Cooperative Research Centre for Oral Health Science, Melbourne Dental School and the Bio21 Institute of Molecular Science and Biotechnology, The University of Melbourne, Victoria, Australia

Received 20 August 2008/ Returned for modification 18 September 2008/ Accepted 22 December 2008

The RgpA-Kgp proteinase-adhesin complexes of Porphyromonas gingivalis were observed, using immunostaining, in human gingival tissue associated with periodontitis but not in healthy tissue. The staining pattern suggested a concentration gradient from the subgingival plaque into the subjacent gingival connective tissue. Intense immunostaining was observed in areas displaying gross disturbance of tissue architecture. P. gingivalis cells and the RgpA-Kgp complexes at low concentrations were shown to stimulate secretory intercellular adhesion molecule 1, interleukin-8 (IL-8), IL-6, and macrophage chemoattractant protein secretion from cultured human epithelial (KB) and fibroblast (MRC-5) cells. However, at high concentrations a reduction in the level of these mediators was observed. In contrast, macrophage inflammatory protein 1{alpha} and IL-1{alpha} were stimulated only at high P. gingivalis cell concentrations. P. gingivalis cells and the RgpA-Kgp complexes were shown to induce apoptosis in KB and MRC-5 cells in a time- and dose-dependent manner. These data suggest that the RgpA-Kgp complexes penetrate the gingival connective tissue; at low concentrations distal from the plaque the complexes stimulate the secretion of proinflammatory mediators, while at high concentrations proximal to the plaque they induce apoptosis and attenuate the secretion of proinflammatory mediators.

* Corresponding author. Mailing address: Centre for Oral Health Science, Melbourne Dental School, Faculty of Medicine, Dentistry and Health Sciences, The University of Melbourne, 720 Swanston Street, Victoria 3010, Australia. Phone: 61 3 9341 1547. Fax: 61 3 9341 1596. E-mail: e.reynolds{at}unimelb.edu.au

{triangledown} Published ahead of print on 29 December 2008.

Editor: B. A. McCormick

{dagger} N.M.O.-S., R.D.P., and G.D.W. contributed equally to this work.

Infection and Immunity, March 2009, p. 1246-1261, Vol. 77, No. 3
0019-9567/09/$08.00+0     doi:10.1128/IAI.01038-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Tam, V., O'Brien-Simpson, N. M., Chen, Y.-Y., Sanderson, C. J., Kinnear, B., Reynolds, E. C. (2009). The RgpA-Kgp Proteinase-Adhesin Complexes of Porphyromonas gingivalis Inactivate the Th2 Cytokines Interleukin-4 and Interleukin-5. Infect. Immun. 77: 1451-1458 [Abstract] [Full Text]  


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