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Infection and Immunity, March 1999, p. 1180-1186, Vol. 67, No. 3
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Activation of Murine Macrophages by Lipoprotein and Lipooligosaccharide of Treponema denticola

Graciela Rosen,1,* Michael N. Sela,1 Ronit Naor,1 Amal Halabi,2 Vivian Barak,3 and Lior Shapira2

Departments of Oral Biology1 and Periodontology,2 Hebrew University-Hadassah Faculty of Dental Medicine, and Department of Oncology, Hadassah Medical Center,3 Jerusalem, Israel

Received 10 July 1998/Returned for modification 8 October 1998/Accepted 8 December 1998

We have recently demonstrated that the periodontopathogenic oral spirochete Treponema denticola possesses membrane-associated lipoproteins in addition to lipooligosaccharide (LOS). The aim of the present study was to test the potential of these oral spirochetal components to induce the production of inflammatory mediators by human macrophages, which in turn may stimulate tissue breakdown as observed in periodontal diseases. An enriched lipoprotein fraction (dLPP) from T. denticola ATCC 35404 obtained upon extraction of the treponemes with Triton X-114 was found to stimulate the production of nitric oxide (NO), tumor necrosis factor alpha (TNF-alpha ), and interleukin-1 (IL-1) by mouse macrophages in a dose-dependent manner. Induction of NO by dLPP was at 25% of the levels obtained by Salmonella typhosa lipopolysaccharide (LPS) at similar concentrations, while IL-1 was produced at similar levels by both inducers. dLPP-mediated macrophage activation was unaffected by amounts of polymyxin B that neutralized the induction produced by S. typhosa LPS. dLPP also induced NO and TNF-alpha secretion from macrophages isolated from endotoxin-unresponsive C3H/HeJ mice to an extent similar to the stimulation produced in endotoxin-responsive mice. Purified T. denticola LOS also produced a concentration-dependent activation of NO and TNF-alpha in LPS-responsive and -nonresponsive mouse macrophages. However, macrophage activation by LOS was inhibited by polymyxin B. These results suggest that T. denticola lipoproteins and LOS may play a role in the inflammatory processes that characterize periodontal diseases.

* Corresponding author. Mailing address: Department of Oral Biology, Faculty of Dental Medicine, the Hebrew University, P.O. Box 12272, Jerusalem 91120, Israel. Phone: 972-2-6758585. Fax: 972-2-6784010. E-mail: grosen{at}pob.huji.ac.il.

Infection and Immunity, March 1999, p. 1180-1186, Vol. 67, No. 3
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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