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Postdoctoral Research Fellow
Address: 3-401 BSB
Phone: (319) 335-7817
Mentor: Wilmara Salgado-Pabón, PhD
Undergraduate Institution: Illinois State University
PhD Institution: University of Iowa
Staphylococcus aureus is the leading cause of infective endocarditis (IE), an infection of the heart endothelium that results in the formation of vegetations comprised of several host factors and bacterial aggregates. It was recently shown that superantigens (SAgs), secreted virulence factors that act as powerful T cell mitogens, play a critical role in the development of multiple S. aureus infections, including IE. While the involvement of SAgs is clear, the underlying mechanism by which SAgs contribute to staphylococcal IE is currently unknown. My current research focuses on one possible mechanism. Specifically, I am studying the direct interaction of two staphylococcal SAgs (TSST-1 and SEC) with human aortic endothelial cells to determine the contribution of this interaction to the perpetuation of IE.
SAgs induce a massive activation of macrophages and CD4 T cells, yet patients with toxic shock syndrome (or patients that recover from toxic shock syndrome) never develop antibodies to SAgs or S. aureus components. Hence, SAgs interfere with the host’s ability to mount an effective immune response. My work will entail studying the effect of superantigenicity on the ability of T cells to respond to their specific antigens.
Kulhankova, K., J.M. King, and W. Salgado-Pabón. 2014. Staphylococcal Toxic Shock Syndrome: Superantigen-Mediated Enhancement of Endotoxin Shock and Adaptive Immune Suppression. Immunol Res 59:182-7.
King, J.M., S. Schesser Bartra, G. Plano, and T.L. Yahr. 2013. ExsA and LcrF Recognize Similar Consensus Binding Sites, but Differences in Their Oligomeric State Influence Interactions with Promoter DNA. J Bacteriol 195:5639-50.
Olson, M.E., J.M. King, T.L. Yahr, and A.R. Horswill. 2013. Sialic acid catabolism in Staphylococcus aureus. J Bacteriol 195:1779-88.
King, J.M., E.D. Brutinel, A.E. Marsden, F.D. Schubot, and T.L. Yahr. 2012. Orientation of Pseudomonas aeruginosa ExsA monomers bound to promoter DNA and base-specific contacts with the P(exoT) promoter. J Bacteriol 194:2573-85.
Brutinel, E.D., J.M. King, A.E. Marsden, and T.L. Yahr. 2012. The distal ExsA-binding site in Pseudomonas aeruginosa type III secretion system promoters is the primary determinant for promoter-specific properties. J Bacteriol 194:2564-72.
Diaz, M.R., J.M. King, and T.L. Yahr. 2011. Intrinsic and Extrinsic Regulation of Type III Secretion Gene Expression in Pseudomonas aeruginosa. Front Microbiol 2:89.
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