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Faculty Detail     Name SUZANNE M MICHALEK   Campus Address BBRB 258B Zip 2170 Phone 205-934-3470 E-mail suemich@uab.edu Other websites

Faculty Appointment(s) Appointment Type Department Division Rank Primary  Microbiology  Microbiology Professor

Graduate Biomedical Sciences Affiliations Cellular and Molecular Biology Program  Immunology  Medical Scientist Training Program  Microbiology

Biographical Sketch  Suzanne M. Michalek is Professor of the Department of Microbiology. Following her initial training in genetics (B.S., 1967; M.S., 1968), she initiated studies in immunology at the University of Chicago with emphasis on the mucosal immune system. Her studies at UAB (Ph.D., 1976) on the induction of salivary IgA antibody responses protective against Streptococcus mutans-induced dental caries provided evidence for the existence of a common mucosal immune system and for the development of a human oral vaccine against dental caries. Following postdoctoral studies at NIH on the effects of bacterial LPS on the host's immune system, she joined the Mucosal Immunology Group at UAB (1979).

Society Memberships Organization Name Position Held Org Link American Academy of Microbiology       American Society for Microbiology       International and American Association for Dental Research       Society for Leukocyte Biology       Society for Mucosal Immunology       The American Association of Immunologists       The International Endotoxin Society

Research/Clinical Interest Title Immunological mechanisms involved in host/microbial interactions, and development of mucosal vaccines against infectious agents Description My research program centers around two major themes: 1) understanding immunological mechanisms involved in host/microbial interactions, with emphasis on host responses to the pathogens Porphyromonas gingivalis and Francisella tularensis, and 2) the development of mucosal vaccines against infectious diseases. P. gingivalis is involved in the development of periodontal disease, an inflammatory process that has also been linked to systemic disorders such as cardiovascular disease. Our studies with P. gingivalis focus on the cell signaling molecules and transcription factors involved in the host response this pathogen. F. tularensis is the cause of tularemia. Due to its ability to infect via multiple routes, its ease of dissemination, and its high infectivity, morbidity and rate of mortality, F. tularensis is considered a bioterrorism agent. The nature of the inflammatory response induced by Francisella infection is a critical determining factor of the outcome of the infectious process. Our studies are directed to delineate the signaling pathways and potential target molecules that could be implicated in the inflammatory process. Through a better understanding of the cellular mechanisms involved in the host immune response to these pathogens, we hope to identify target molecules for the development of protective immunotherapeutic approaches. Since greater than 95% of all infectious disease involve the colonization or penetration of our mucosal surfaces, our mucosal immune system serves as our first line of defense against pathogens. Therefore, we have devoted considerable effort to understanding the mucosal immune system and in developing mucosal vaccines against microbial pathogens. Current in vivo studies in adults and children are testing the effectiveness of our mucosal vaccine consisting of recombinant microbial polypeptides from Streptococcus mutans (the principle etiologic agent of tooth decay) in inducing mucosal as well as systemic immune responses that protect against dental caries. We have also developed a mucosal vaccine that confers greater than 80% protection against respiratory infection by the biologic threat agent F. tularenesis. These studies are being done in a murine model. Ongoing studies are designed to test the effectiveness of our vaccine in protecting against highly virulent forms of this pathogen and in additional model systems. We also plan on determining the effectiveness of our vaccine in the elderly, since it is well know that age does affect our immune system, making us more susceptible to diseases. It is possible that our vaccine may need to be modified by including additional antigens/adjuvants to make it even more effective in inducing protective responses in the population at large. Our studies should help in the development of means to treat/prevent infectious diseases via therapeutic approaches and/or mucosal vaccines. Since microbial pathogens, e.g., P. gingivalis, can alter the outcome of systemic diseases, such as kidney disease, cancer or depression, we are also investigating the cellular mechanisms involved in these processes in an effort to define therapeutic approaches that would help in the treatment of systemic diseases/disorders.

Selected Publications  Publication PUBMEDID Yang, D., Chen, Q., Su, S.B., Zhang, P., Kurosaka, K., Caspi, R.R., Michalek, S.M., Rosenberg, H.F., Zhang, N., and Oppenheim, J.J. 2008. Eosinophil-derived neurotoxin acts as an alarmin to activate the TLR2-MyD88 signal pathway in dendritic cells and enhances Th2 immune responses. J. Exp. Med. 205: 79-90.    Seo, H., Michalek, S.M., and Nahm, M.H. 2008. Lipoteichoic acid is important in innate immune responses to gram-positive bacteria. Infect. Immun. 76: 206-213.    Cole, L.E., Shirey, K.A., Barry, E., Santiago, A., Rallabhandi, P., Elkins, K.L., Puche, A., Michalek, S.M., and Vogel, S.N. 2007. TLR2-mediated signaling requirements for Francisella tularensis LVS infection of murine macrophages. Infect. Immun. 75: 4127-4137.    Zhang, P., Lewis, J.P., Michalek, S.M., and Katz, J. 2007. Role of CD80 and CD86 in host immune responses to the recombinant hemagglutinin domain of Porphyromonas gingivalis gingipain and in the adjuvanticity of cholera toxin B and monophosphoryl lipid A. Vaccine 25: 6201-6210.    Banas, J.A., Miller, J.D., Fuschino, M.E., Hazlett, K.R.O., Toyofuku, W., Porter, K.A., Reutzel, S.B., Florczyk, M.A., Mc Donough, K.A., and Michalek, S.M. 2007. Evidence that accumulation of mutants in a biofilm reflects natural selection rather than stress-induced adaptive mutation. Appl. Environ. Microbiol. 73: 357-361.    Childers, N.K., Li, F., Dasanayake, A.P., Li, Y., Kirk, K., Michalek, S.M. 2006. Immune response in humans to a nasal boost with Streptococcus mutans antigens. Oral Microbiol. Immunol. 21:309-313.    Salam, M.A., Katz, J., Zhang, P., Hajishengallis, G., and Michalek, S.M. 2006. Immunogenicity of Salmonella vector vaccines expressing SBR of Streptococcus mutans under the control of a T7-nirB (dual) promoter system. Vaccine 24:5003-15.    Cole, L.E., Elkins, K.L., Michalek, S.M., Qureshi, N., Eaton, L.J., Rallabhandi, P., Cuesta, N., and Vogel, S.N. 2006. Immunologic consequences of Francisella tularensis live vaccine strain infection: role of the innate immune response in infection and immunity. J. Immunol. 176:6888-6899.    Katz, J., Zhang, P., Martin, M., Vogel, S.N., and Michalek, S.M. 2006. Toll-like receptor 2 is required for inflammatory responses to Francisella tularensis LVS. Infect. Immun. 74:2809-2816.    Han, S.H., Kim, J.H., Martin, M., Chung, G-H., Michalek, S.M., and Nahm, M.H. 2005. Lipoteichoic acid-induced nitric oxide production depends on the activation of PAF receptor and Jak2. J. Immunol.176:573-579.    First Prev   1 2 3 of  3  Next Last

Keywords mucosal vaccines, inflammation, TLRs, T cell, cytokines, signaling pathways

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