Jacques Izard, PhD

Treponema denticola is a consensus periodontal pathogen. Recent studies have also associated Treponema bacteria with root canal/endodontic infections in humans. T. denticola pathogenicity is not yet well understood. The stringent growth requirements for T. denticola in the laboratory and a delayed development of a genetic system has impaired research progress until recently.

Treponemal cell division and motility are key to tissue invasion, population expansion, and persistence in a host. Two related filamentous structures, playing a role in the pathogenicity of Treponema bacteria, are the focus of the laboratory. The flagellar filaments, source of the organism's motility, are uniquely positioned in the periplasmic space of Treponema cells. Their mode of motion facilitates tissue penetration, allowing the bacteria to be at the forefront of infection.

The cytoplasmic filament bundle is involved in the treponemal cell division cycle and has an unique structural organization. Cytoplasmic bridging proteins connect the filaments, maintaining the distance between them and providing the overall ribbon-like structure. The filaments are anchored by proteins associated with the inner cell membrane. Each filament is composed of a unique monomer, the cytoplasmic filament protein A (CfpA). CfpA is a member of a bacterial intermediate-like filament family.

Genetically engineered treponemal cells are used to understand the pathogen's interaction with the host. Our previous results indicate that T. denticola has high pathogenicity based on bone loss in an experimental endodontic infection model. The bacteria disseminate to distant organs in immunodeficient, and to a lesser extent in immunocompetent animals, further substantiating their potential importance in oral and extraoral conditions. We are currently investigating the role of key components of the cell biology in the tissue invasion and persistence of treponemal bacteria in the host.
 

Selected Publications

Izard J., Hsieh CE, Limberger RJ, Mannella CA, Marko M. 2008. Native cellular architecture of  Treponema denticola  revealed by cryo-electron tomography. J. Struct Biol. 163(1):10-17.

 Izard J. 2006. Cytoskeletal cytoplamic filament ribbon of treponema: A member of an intermediate-like filament protein family. J. Mol. Microbiol. Biotechnol. 11(3–5) :159-1 66.

Foschi F, Izard J, Sasaki H, Sambri V, Prati C, Stashenko P. 2006. Treponema denticola in disseminating endodontic infections. J. Dent. Res. 85(8):761 –765.

Tanner ACR, Izard J. 2006. Tannerella forsythia, a periodontal pathogen entering the genomic era. Periodontol. 2000 42 (1) :88–113.

Izard J, Limberger RJ. 2006. Structural and genomic features of treponemal artchitecture. In: Radolf JD, Lukehart SA. (eds). Treponema: Molecular and Cellular Biology. Chapter 3, pp. 41–62. England. Horizon Bioscience/Caister Academic Press.

Izard J, Hsieh CE, Mannella CA, Limberger RJ, and Marko M. 2005. Periplasm organization in Treponema denticola as studied by cryo-electron tomography. Microsc. Microanal. 11(Suppl. 2) :340–341.

Izard J, McEwen BF, Barnard RM, Portuese T, Samsonoff WA, Limberger RJ. 2004. Tomographic reconstruction of treponemal cytoplasmic filaments reveals novel bridging and anchoring components. Mol. Microbiol. 51(3):609–618.

Slivienski-Gebhardt L, Izard J, Samsonoff WA, Limberger RJ. 2004. Development of a novel chloramphenicol-resistance expression plasmid used for genetic complementation of a fliG-deletion mutant of Treponema denticola. Infect. Immun. 72(9):5493–5497.

Izard J, Samsonoff WA, Limberger RJ. 2001. Cytoplasmic filament-deficient mutant of Treponema denticola has pleiotropic defects. J. Bacteriol. 183(3) :1078–1084.

Staff

Research Assistant

Oxana V. Baranova