Assistant Professor Departments of Microbiology
Center for Microbial Interface Biology
541 Biological Sciences Building
484 West 12th Avenue
Columbus, Ohio 43210-1292
Phone: (614) 247-7671
Fax: (614) 292-8120
Dr. Seveau’s research is focused on understanding, at the molecular level, host-pathogen interactions and the innate immune responses to infection. The results of her research provide a molecular basis for the logical design of new anti-microbial therapeutics. Specific projects currently are to:
Establish how Listeria monocytogenes invades and establishes infections of mammalian cells and tissues. L. monocytogenes is a food-borne intracellular bacterial pathogen that causes gastroenteritis, meningitis, encephalitis and fetal infections of humans. L. monocytogenes lives inside host cells, and its ability to invade mammalian cells facilitates both its initial transit through the epithelial barrier of the digestive tract, and subsequent colonization of many internal organs. State-of-the-art quantitative fluorescence microscopy is used as the primary approach to investigate and quantify L. monocytogenes infections of live host cells. The complex dynamics of the signaling events that lead to L. monocytogenes uptake by epithelial cells and macrophages are being determined and characterized.
Determine the molecular basis, and outcome of host-cell signaling induced by cholesterol-dependent cytolysin (CDCs) toxins. CDCs are a family of closely-related pore-forming bacterial toxins produced by many Gram-positive Listeria, Streptococcus, Bacillus and Clostridium species. At concentrations below those that cause host-cell lysis, these virulence factors function as signaling molecules but the underlying molecular biology and the host cell responses to this toxin-signaling remain unknown. To gain this information, we are investigating the signaling properties of listeriolysin O, a CDC and the major virulence factor of L. monocytogenes. Structure-function dissection of listeriolysin O is being combined with live-cell imaging to establish how this toxin affects host-cell signaling during the course of a bacterial infection.