Menu UF Health Home Menu
 

Shannon Wallet, Ph.D.

Dr. Shannon Wallet

Department of Periodontology

Associate Professor

Phone: 352-273-8370
Laboratory: 352-273-8135
Email: swallet@dental.ufl.edu
Room D11-15
PO Box 100434
Gainesville, FL 32610-0434

Education

  • UNC at Chapel Hill, Chapel Hill, NC: Ph.D. – Curriculum of Oral Biology, 2000-2005
  • Duke University, Durham, NC: Clinical Laboratory Science Certification, 1994-1995
  • North Carolina State University, Raleigh, NC: Bachelor 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: Ph.D. 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
    Principal 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)
  • 09/06-06/13: Assistant Professor University of Florida-Department of Periodontology
    Department Chair: Ikramuddin Aukhil, B.D.S., M.S.
  • 07/13-present: Associate Professor University of Florida-Department of Periodontology

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

  • Wallet, M.A., S.M. Wallet, M. J.W. Sleasman, M.M. Goodenow. IFNγ primes macrophages for inflammatory activation by high molecular weight hyaluronan. Cellular Immunology. In press. March 2010.
  • Verma, R., I. Bhattacharyya, A. Sevilla, I. Lieberman, S. Pola, M. Nair, S.M. Wallet, I. Aukhil, and K.N. Lakshmyya. Porphyromonas gingivalis and Treponema denticola mixed microbial infection in a rat model of periodontal disease. Interdisciplinary Perspectives on Infectious Disease. In press March 2010.
  • Meka, A, V. Bakthavatchalu, S. Sathishkumar, C. M. Lopez, R. K. Verma, S. M. Wallet, I. Bhattacharyya, B. F. Boyce, M. Handfield, R. Lamont, H. V. Baker, J.L. Ebersole, and L. Kesavalu. Molecular characterization of Treponema denticola infection-induced bone and soft tissue transcriptional profiles. Mol.Oral. Microbiol. In press February 2010.
  • Shaddox, L., J. Wiedey*, E. Bimstein, I. Magnuson, M. Clare-Salzler, I. Aukhil, and S. M. Wallet. Hyper-Responsive Phenotype in Localized Aggressive Periodontitis. Journal of Dental Research. 89(2): 143-8; Feb (2010).
  • Pauley, K.M., M. Satoh, P.R. Dominguez-Gutierrez, S.M. Wallet, L.S. Holliday, W.H. Reeves, and E.K.L. Chan. Formation of GW/P bodies as marker for microRNA-mediated regulation of innate immune signaling. Immunol.Cell Bio. Feb;88(2);205-12 (2010) Kata, J, S.M. Wallet, and S. Cha. Periodontal Disease and Oral-Systemic Connection: Its all the RAGE. Quintessence International. In press July 2009.
  • Tesmer, M., S.M. Wallet, T. Koutouzis, T. Lundgren. Bacterial Colonization of the Dental Implant Fixture-Abutment Interface: An In-vitro Study. Journal of Periodontology. 80 (12): (2009).
  • Mans, J.J, K. von Lackum, S. Willis, C. Dorsey, S.M. Wallet, H.V. Baker, R. J. Lamont and M. Handfield. The degree of complexity of a microbiota challenge modulates the epithelial response to infection. BMC Genomics. 18;10:380 (2009).
  • Koutouzis, T., D. Haber^, L. Shaddox, I. Aukhil, and S. M. Wallet. Reactivity of serum total Ig Antibodies to Periodontal Host Tissue Components: A Pilot Study. Journal of Periodontology. 80(4): 625-33 (2009).
  • Yan, Xiu, C.P. Wong, Y. Hamaguchi, Y. Wang, S.M. Pop, R.M. Tisch, and T.F. Tedder. B Lymphocytes Depletion by CD20 Monoclonal Antibody Prevents Diabetes in NOD mice Despite Isotype-Specific Differences in FcγR Effector Function. Journal of Immunology. 180, 2863-2875. (2008).
  • 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 ß cell autoimmunity. Diabetes. Vol 56 pp. 1395-1402 (2007).
  • 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).
  • 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).
  • 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).
  • 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).
  • 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
  • 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).

* indicates mentored DMD student, ^ indicates mentored COD-MS