Periodontology
Dr. Shannon Wallet
Periodontics
Assistant Professor
Phone: 352-392-9983
Laboratory: 352-273-8370
E-mail: swallet@dental.ufl.edu
Room D11-15
PO Box 100434
Gainesville, FL 32610-0434
UNC at Chapel Hill, Chapel Hill, NC
PhD. - Curriculum of Oral Biology, 2000-2005
Duke University, Durham, NC
Clinical Laboratory Science Certification, 1994-1995
North Carolina State University, Raleigh, NC
Bachelors of Science - Medical Technology, 1991-1995
Previous positions
1995-2000 Medical Technologist Duke University Medical Center
Supervisor: Mary Lee Campbell, MT (ASCP) Transfusion Services Laboratory
1999-2000 Research Assistant Duke University Medical Center
Supervisor: Nancy Reinsmoen, PhD. Immunology Transplant Laboratory
2000-2005 PhD. Candidate University of North Carolina at Chapel Hill
Dissertation advisor: Roland Tisch, PhD. Department of Microbiology and Immunology
04/05-11/05 Post-doctoral Fellow University of Pittsburgh School of Medicine
Principle Investigator: Chad Steele, PhD. Department of Pediatrics
11/05-08/06 Scientific Consultant University of North Carolina at Chapel Hill
Dental Research Center (DRC), Comprehensive Center for Inflammatory Disease (CCID)
09/06-present Assistant Professor University of Florida-Department of Periodontology
Department Chair Person: Ikramuddin Aukhil, BDS, MS
Main interests
Our research broadly focuses on the innate immune responses in both Type 1 and Type 2 diabetics with the understanding that these are similar diseases with different mechanisms leading to manifestation. Our initial interests involve the interactions of the diabetic host with mucosal pathogens and how these interactions contribute to the disease process of diabetes as well as how diabetic host responses differ from that of a normoglycemic host. Finally, we are interested in how these potentially aberrant innate immune responses may affect other disease processes which have been classified as secondary complications of diabetes, such as periodontitis, cardiovascular disease, and arthritis. We have several current projects which are beginning to help us investigate these areas.
One such project involves the fact that few differences in microflora responsible for periodontitis are found between diabetic and non-diabetic patients. Ye, pathogens do respond to stimuli within the host resulting in alteration of gene expression, marked by changes in in vivo-induced-antigens, to optimize their survival contributing to the pathogenicity of organisms. Although the diabetic periodontal micro-environment differs from a normoglycemic host, investigation into the affect on in vivo-induced-antigens has not been explored. We hypothesize that in vivo-induced-antigens of pathogenic and commensal oral bacteria differ in a diabetic population with periodontal disease compared to a normoglycemic population.
A second project proposes that gingival epithelia cells (GEC), first barriers against oral pathogens, have immune function. We hypothesize that diabetogenic GEC have aberrant immunological functions. In diabetics a ‘hyper-responsive’ phenotype has been described in multiple immune cells such as macrophages. GEC have many of the same immunological characteristics yet their role in ‘hyper-responsiveness trait’ has not been elucidated. Therefore, it is the goal of this proposal to define the role of GEC in the innate immune response to periodontitis as well as determine intrinsic defects of diabetogenic GEC. These data will improve the understanding of diabetic innate immune mechanisms. Importantly, these studies will lay the groundwork for investigation of specific alterations in innate immune function of not only GEC, but other mucosal epithelial and endothelial sites. Ultimately these studies will lead to the development of better primary prevention strategies to reduce the diabetic complication of periodontitis allowing for improved glycemic control in diabetic individuals.
Selected Publications
1. Scott, R. S., E.J. McMahon, S.M. Pop, E.A. Reap, R. Caricchio, P.L. Cohen, H. S. Earp, and G. K. Matsushima. Phagocytosis and clearance of apoptotic cells is mediated by MER. Nature. 411, 207-211. (2001).
2. Seifarth, C.*, S.M. Pop*, B. Liu, C.P. Wong and R. Tisch. More stringent conditions of plasmid DNA vaccination are required to protect grafted versus endogenous islets in nonobese diabetic mice. Journal of Immunology. 170, 469-476. (2003). *co-first authorship
3. Pop, S.M., D. A. Culton, S.H. Clarke, and R. Tisch. Progression of autoimmune diabetes in NOD mice involves diminishing numbers of FoxP3-expressing CD4+CD25+ T cells. Journal of Experimental Medicine. 201 (8), 1333-1346. (2005).
4. Steele, C., R. Rapaka, A. Metz, S.M. Pop, D.L. Williams, S. Gordon, J.K. Kolls and G.D. Brown. The beta glucan receptor Dectin-1 recognizes specific morphologies of Aspergillus fumigatus. PLoS Pathogens. 1 (4), e42, 0323-0334. (2005).
5. Pop, S.M., J.K. Kolls and C. Steele. Pneumocystis: carbohydrate recognition and innate immunity. International Journal of Biochemistry and Cell Biology. Review 38 (1), 17-22. (2006).
6. Maile, R., S.M. Pop, R. Tisch, E. J. Collins, B.A. Cairns, and J. A. Frelinger. Low-avidity CD8lo T cells induced by incomplete antigen stimulation in vivo regulate naïve higher-avidity CD8hi T cell responses to the same antigen. European Journal of Immunology. 36 (2), 397-410. (2006).
7. Pop, S.M., C.P. Wong, Q. He, Y. Wang, M. Wallet, K. Goudy, J. Staton, and R. Tisch. The type and frequency of immunoregulatory CD4+ T cells determine the efficacy of suppressing recurrent β cell autoimmunity. Diabetes. 56 (5), 1395-1402 (2007)
