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Infection and Immunity, October 2001, p. 6276-6283, Vol. 69, No. 10
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.10.6276-6283.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Motility and Chemotaxis in Tissue Penetration of Oral Epithelial Cell Layers by Treponema denticola

Renate Lux,1 James N. Miller,2 No-Hee Park,1 and Wenyuan Shi1,*

School of Dentistry and Molecular Biology Institute1 and Department of Microbiology, Immunology, and Molecular Genetics,2 University of California, Los Angeles, California 90095-1668

Received 29 May 2001/Returned for modification 18 June 2001/Accepted 22 July 2001

The ability to penetrate tissue is an important virulence factor for pathogenic spirochetes. Previous studies have recognized the role of motility in allowing pathogenic spirochetes to invade tissues and migrate to sites favorable for bacterial proliferation. However, the nature of the movements, whether they are random or controlled by chemotaxis systems, has yet to be established. In this study, we addressed the role of motility and chemotaxis in tissue penetration by the periodontal disease-associated oral spirochete Treponema denticola using an oral epithelial cell line-based experimental approach. Wild-type T. denticola ATCC 35405 was found to penetrate the tissue layers effectively, whereas a nonmotile mutant was unable to overcome the tissue barrier. Interestingly, the chemotaxis mutants also showed impaired tissue penetration. A cheA mutant that is motile but lacks the central kinase of the chemotaxis pathway showed only about 2 to 3% of the wild-type penetration rate. The two known chemoreceptors of T. denticola, DmcA and DmcB, also appear to be involved in the invasion process. The dmc mutants were actively motile but exhibited reduced tissue penetration of about 30 and 10% of the wild-type behavior, respectively. These data suggest that not only motility but also chemotaxis is involved in the tissue penetration by T. denticola.

* Corresponding author. Mailing address: School of Dentistry and Molecular Biology Institute, University of California, Los Angeles, CA 90095-1668. Phone: (310) 825-8356. Fax: (310) 794-7109. E-mail: wenyuan{at}ucla.edu.

Infection and Immunity, October 2001, p. 6276-6283, Vol. 69, No. 10
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.10.6276-6283.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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