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Infection and Immunity, February 2009, p. 694-698, Vol. 77, No. 2
0019-9567/09/$08.00+0 doi:10.1128/IAI.01004-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Department of Applied Oral Sciences,1 Department of Dental Clinical Sciences, Faculty of Dentistry,2 Department of Microbiology and Immunology,3 Department of Pediatrics, Faculty of Medicine, Dalhousie University,4 Canadian Center for Vaccinology,5 Proteomics and Mass Spectrometry Centre, Dalhousie University and the IWK Health Centre, Halifax, Nova Scotia, Canada6
Received 11 August 2008/ Returned for modification 15 September 2008/ Accepted 6 November 2008
Treponema denticola is considered to be an agent strongly associated with periodontal disease. The lack of an animal infection model has hampered the understanding of T. denticola pathogenesis and the host's immune response to infection. In this study, we have established an oral infection model in mice, demonstrating that infection by oral inoculation is feasible. The presence of T. denticola in the oral cavities of the animals was confirmed by PCR. Mice given T. denticola developed a specific immune response to the bacterium. The antibodies generated from the infection were mainly of the immunoglobulin G1 subclass, indicating a Th2-tilted response. The antibodies recognized 11 T. denticola proteins, of which a 62-kDa and a 53-kDa protein were deemed immunodominant. The two proteins were identified, respectively, as dentilisin and the major outer sheath protein by mass spectrometry. Splenocytes cultured from the infected mice no longer produced interleukin-10 and produced markedly reduced levels of gamma interferon relative to those produced by naïve splenocytes upon stimulation with T. denticola. Mandibles of infected mice showed significantly greater bone resorption (P < 0.01) than those of mock-infected controls.
Published ahead of print on 17 November 2008.
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