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Infection and Immunity, July 2001, p. 4493-4501, Vol. 69, No. 7
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.7.4493-4501.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Porphyromonas gingivalis Gingipain-R Enhances Interleukin-8 but Decreases Gamma Interferon-Inducible Protein 10 Production by Human Gingival Fibroblasts in Response to T-Cell Contact

Mari Oido-Mori,1,2 Roger Rezzonico,3 Pao-Li Wang,4 Yusuke Kowashi,2 Jean-Michel Dayer,3 Pierre C. Baehni,1 and Carlo Chizzolini3,*

Department of Preventive Dentistry, School of Dental Medicine, University of Geneva,1 and Division of Immunology and Allergy, Department of Internal Medicine, Geneva University Hospital,3 1211 Geneva 14, Switzerland, and Department of Pharmacology, Osaka Dental University, Hirakata 573-1121 Osaka,4 and Department of Periodontology and Endodontology, School of Dentistry, Health Sciences University of Hokkaido, 1757 Kanazawa, Ishikari-Tobetsu, 061-0293 Hokkaido,2 Japan

Received 7 February 2001/Returned for modification 27 March 2001/Accepted 16 April 2001

Proteases produced by Porphyromonas gingivalis, an oral pathogen, are considered important virulence factors and may affect the responses of cells equipped with proteinase-activated receptors. The aim of this study was to investigate the effect of the arginine-specific cysteine protease gingipain-R produced by P. gingivalis on chemokine production by human gingival fibroblasts (HGF) and the effect of gingipain-R treatment on the subsequent contact-dependent activation of HGF by T cells. HGF incubated in the presence of purified 47-kDa gingipain-R showed increased levels of interleukin-8 (IL-8) mRNA. Cyclooxygenase-2 (COX-2) mRNA was also induced. Further exposure of HGF to activated T cells resulted in the dose- and time-dependent enhancement of IL-8 transcription and release. T-cell membrane-bound tumor necrosis factor (TNF) was the ligand inducing IL-8 production by HGF, since TNF neutralization abrogated HGF responses to T-cell contact. The enhanced IL-8 release was due, at least in part, to prostaglandin-E2 production, which was mostly blocked by indomethacin. Gingipain-R proteolytic activity was required since heat inactivation, specific synthetic protease inhibitors, and the natural substrate competitor histatin 5 abrogated its effects. The enhanced production of IL-8 in response to T-cell contact was specific since monocyte chemotactic protein-1 (MCP-1) production was unaffected while interferon-gamma-inducible protein-10 (IP-10) was inhibited. The sum of these activities may result in the recruitment of differential cell types to sites of inflammation since IL-8 preferentially recruits neutrophils and IP-10 attracts activated T cells and may be relevant to the pathogenesis of periodontitis.

* Corresponding author. Mailing address: Division of Immunology and Allergy, Geneva University Hospital, 1211 Geneva 14, Switzerland. Phone: 41 22 372 9370. Fax: 41 22 372 9418. E-mail: chizzoli{at}cmu.unige.ch.

Infection and Immunity, July 2001, p. 4493-4501, Vol. 69, No. 7
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.7.4493-4501.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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