
| Administration | Basic Sciences | Clinical Sciences | Centers of Excellence |
|---|---|---|---|
|
|
|
Zezhang Tom Wen, Ph.D.
Assistant Professor
1100 Florida Avenue, Room 6305
|
| Degrees |
Ph.D., Molecular Microbiology, 1998 |
| Research Interests |
The primary interests of my research are in molecular characterization of biofilms and identification of novel targets for therapy and vaccine development against biofilm-associated diseases. In nature, bacteria exist in highly complex multiple-species communities, better known as biofilms. Due to their increased tolerance to host defense, antibiotic therapies and other antibacterial agents biofilms are notoriously difficult to eliminate and are a source of many recalcitrant infections. A better understanding of the processes underlying biofilm formation and persistence should ultimately lead to the development of novel and effective therapeutic and preventive strategies for diseases (such as dental caries, periodontitis and cystic fibrosis) and conditions (e.g., fouling of catheters) in which biofilm formation plays a prominent role. Currently, Streptococcus mutans, the primary etiological agent of human dental caries, serves as the model microorganism. Major effort is directed, but not limited to: (1) microbial cell-cell communication and its impact on establishment, persistence and competitiveness of S. mutans using continuous, mixed-species biofilm models and confocal laser scanning microscopy; (2) identification and characterization of genes required for biofilm formation by S. mutans, including further characterization of BrpA, a glycoprotein with major roles in environmental stress tolerance and formation of biofilms by S. mutans, focusing on the role and the underlying mechanisms in BrpA in regulation of S. mutans pathogenicity and the potential for targeting BrpA in anti-caries strategy. |
| Selected Publications |
Ahn, S-J, Ahn, S. J., Wen, Z. T., Brady, L. J., and Burne, R. A. 2008. Characteristics of biofilm formation by Streptococcus mutans in the presence of saliva. Infect. Immun. (Accepted). Abranches, J., Nascimento, M. M., Zeng, L., Browngardt, C. M., Wen, Z. T., Rivera, M. F., and Burne, R. A. 2008. CcpA regulates central metabolism and virulence gene expression in Streptococcus mutans. J. Bacteriol. 190(7):2340-9 Ahn, S. J., Wen, Z. T., and Burne, R. A. 2007. Effects of oxygen on virulence traits of Streptococcus mutans. J. Bacteriol. 189(23):8519-27. Zeng, L., Wen, Z. T., and Burne, R. A. 2006. A novel signal transduction system and feedback loop regulate fructan hydrolase gene expression in Streptococcus mutans. Mol. Microbiol. 62(1):187-200. Abranches, J., Candella, M. M., Wen, Z. T., Baker, H. V., and Burne, R. A. 2006. Different roles of EIIABMan and EIIGlc in regulation of energy metabolism, biofilm development, and competence in Streptococcus mutans. J. Bacteriol. 188(11):3748-56. Wen Z. T., Baker, H. V., and Burne, R. A. 2006. Influence of BrpA on critical virulence attributes of Streptococcus mutans. J. Bacteriol. 188(8):2983-92. Ahn, S. J., Wen, Z. T., and Burne, R. A. 2006. Multilevel control of competence development and stress tolerance in Streptococcus mutans UA159. Infect. Immun. 74(3):1631-42. Wen, Z. T., Suntharaligham, P., Cvitkovitch, D. G., and Burne, R. A. 2005. Trigger factor in Streptococcus mutans is involved in stress tolerance, competence development, and biofilm formation. Infect. Immun. 73(1), 219-25. Tanzer, J. M., Thompson, A., Wen, Z. T., and Burne, R. A. 2006. Fructose Transport, Xylitol Resistance, and Virulence. J. Dent. Res. 85(4):369-371 Browngardt, C. M., Wen, Z. T., and Burne, R. A. 2004. RegM is required for optimal fructosyltransferase and glucosyltransferase gene expression in Streptococcus mutans. FEMS Microbiol. Lett. 240(1), 75-9. Wen, Z. T., and Burne, R. A. 2004. LuxS-mediated signaling in Streptococcus mutans is involved in regulation of acid and oxidative stress tolerance and biofilm formation. J. Bacteriol. 186(9), 2682-91. Wen, Z. T., Peng, L., and Morrison, M. 2003. The glutamine synthetase of Prevotella bryantii B(1)4 is a family III enzyme (GlnN) and glutamine supports growth of mutants lacking glutamate dehydrogenase activity. FEMS Microbiol. Lett. 229(1), 15-21. Wen, Z. T., and Burne, R. A. 2002. Functional genomics approach to identifying genes required for biofilm development by Streptococcus mutans. Appl. Environ. Microbiol. 68(3), 1196-203. Erratum in: Appl. Environ. Microbiol. 69(1), 722. Wen, Z. T., and Burne, R. A. 2002. Analysis of cis- and trans-acting factors involved in regulation of the Streptococcus mutans fructanase gene (fruA). J. Bacteriol. 184(1), 126-33. Wen, Z. T., Browngardt, C., and Burne, R. A. 2001. Characterization of two operons that encode components of fructose-specific enzyme II of the sugar:phosphotransferase system of Streptococcus mutans. FEMS Microbiol. Lett. 205(2), 337-42. Wen, Z. T., and Burne, R. A. 2001. Construction of a new integration vector for use in Streptococcus mutans. Plasmid, 45(1), 31-6. Burne, R. A., Wen, Z. T., Chen, Y. Y., and Penders, J. E. 1999. Regulation of expression of the fructan hydrolase gene of Streptococcus mutans GS-5 by induction and carbon catabolite repression. J. Bacteriol. 181(9), 2863-71. Wen, Z. T., and Morrison, M. 1997. Glutamate dehydrogenase activity profile for the type strains of Prevotella spp. Appl. Environ. Microbiol. 64:3314-17. Wen, Z. T., and Morrison, M. 1996. The NAD(P)H-dependent glutamate dehydrogenase activities of Prevotella ruminicola B14 can be attributed to one enzyme (GdhA), and ghdA expression is |