Juliane Bubeck-Wardenburg

Email: jbubeck@peds.bsd.uchicago.edu

Julie received her M.D. and Ph.D. degree in Immunology from Washington University in St. Louis in 2001. Her graduate studies in the laboratory of Dr. Andrew Chan served to identify the first in vivo substrate of the T cell receptor complex-associated kinase ZAP-70, demonstrating that this substrate plays an essential role in coordinating the signaling cascades that emanate from the activated receptor. Following the completion of this joint program, Julie then pursued clinical training in General Pediatrics and Pediatric Critical Care at the University of Chicago. During this time, she developed an interest in understanding the pathogenesis of Staphylococcus aureus infection, prompting her to join the laboratory of Dr. Olaf Schneewind in the Department of Microbiology at the University of Chicago as a Pediatric Scientist Development Program Fellow. Her post-doctoral research in the Schneewind lab focused on the development of an animal model of Staphylococcus aureus pneumonia, which was utilized to define bacterial virulence factors that are central to the pathogenesis of lung infection. Julie joined the faculty in the Departments of Pediatrics and Microbiology at the University of Chicago in 2008.

Julie’s laboratory maintains a strong interest in understanding the host-pathogen interaction during the course of S. aureus lung infection. In particular, the lab is currently investigating the molecular mechanisms by which critical virulence factors effect injury of host cells, while using a genomics-based approach to define the host response to S. aureus-mediated lung injury. These approaches are paired with studies aimed at identifying the host genetic factors that govern susceptibility/resistance to disease. The ultimate goal of these investigations is to shed light on strategies that may disrupt the host-pathogen interaction, thereby contributing to the design of novel preventative and therapeutic approaches to combat S. aureus pneumonia. As a number of bacterial pathogens demonstrate trophism for the human lung, it is anticipated that the knowledge gained from these studies may facilitate a broader understanding of the mechanisms that underlie pathogen-associated lung injury.