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John-Demian (JD) Sauer

Picture of John-Demian (JD) SauerAssistant Professor of Medical Microbiology & Immunology
4203 Microbial Sciences Building
1550 Linden Drive
Office: (608) 263-1529
Laboratory: 263-4230
Email: sauer3@wisc.edu
Overview · Personnel · Publications · Lab Website

Education

1998-2002, B.S. Biology, Cornell University, Ithaca, NY
2002-2006, Ph.D. Microbiology and Immunology, Dr. Michele Swanson's Lab, University of Michigan, Ann Arbor, MI
2006-2011, Postdoctoral Fellow, Dr. Daniel Portnoy's Lab, University of California, Berkeley, CA

Areas of Study

Bacterial Pathogenesis, Immunology

Research Overview

Our lab is interested in how intracellular pathogens parasitize host cells and how the host, in turn, recognizes these pathogens and defends against them. We use the bacterium Listeria monocytogenes, a Gram positive foodborne pathogen, as a model organism to address these questions. L. monocytogenes is capable of infecting a wide variety of cell types, including professional phagocytes such as macrophages and dendritic cells. Survival from infection with L. monocytogenes results in the development of robust and long term protective cell mediated immunity. To understand the complex game of tug and war between the bacteria and the host, we utilize genetics, both in the pathogen and in the host, to determine the factors necessary to promote disease (pathogen) and immunity (host).

Random mutagenesis of L. monocytogenes, utilizing transposons, allows us to screen for bacterial factors that the pathogen utilizes to parasitize normally bactericidal macrophages. These screens have highlighted the importance of specific central metabolism and cell wall biosynthesis pathways in the pathogenesis of L. monocytogenes. Similarly, transposon mutagenesis has allowed us to identify bacterial factors that impact innate immune recognition by the host. In particular we have identified bacterial mutants that both hyper- and hypo-induce various innate immune signaling pathways, specifically the inflammasome and a cytosolic type I IFN induction pathway. We use these bacterial mutants both to understand the downstream host signaling pathways and the ligands that trigger them.

Finally, we use the well defined ex vivo and in vivo murine Listeriosis models to understand the role of specific innate immune signaling pathways during infection by intracellular pathogens. Specifically, we utilize cells/mice lacking innate immune signaling molecules, in combination with L. monocytogenes mutants, to determine the role of inflammasome activation and type I interferon induction during acute infections and the development of long term immunity.

Our long term goals are to understand the mechanisms by which intracellular pathogens parasitize host cells and how the host defends against these pathogens. In addition, we are interested in continuing to develop L. monocytogenes as an immunotherapeutic platform.