Research Interests Host-pathogen interactions, genomic approaches to gene expression analysis, tuberculosis immune evasion and therapeutics. Our research focuses on the human innate immune system after infection using a variety of genomic and immunologic technologies. The goals of the research are to understand normal immune defenses and the pathogenesis of specific microorganisms, ultimately to develop clinically useful diagnostics and therapeutics. We have studied the effects of a variety of organisms, including Staphylococcus aureus, Listeria monocytogenes, Salmonella typhi and typhimurium, Escherichia coli, and Mycobacterium tuberculosis, on human macrophage gene expression with high density DNA microarrays. These studies have shown that human innate immune cells express an activation program of genes irrespective of the type of bacterium that is encountered. Host cell gene expression signatures have comparatively few specific alterations induced by specific bacteria. And yet, these specific alterations provide insight into mechanisms of pathogenesis of these infectious agents. Our lab is now applying this research strategy to biodefense agents, in particular Francisella tularensis, a category A agent whose pathogenesis is intimately tied to macrophages. Using gene expression profiling, we expect to identify how these organisms alter normal activation events, allowing them to propagate and cause disease. Our lab also continues the study of immune evasion strategies of Mycobacterium tuberculosis, with the goal of immune intervention and vaccination. We have been investigating the molecular signature of the granulomas from the lungs of infected monkeys. We also have an active program in immune modulation against infection using cytokines.   Selected Publications Lu Y, Rosenfeld R, Simon I, Nau GJ, Bar-Joseph Z. A probabilistic generative model for GO enrichment analysis. Nucleic Acids Res. 2008 Aug 1. Turnquist HR, Sumpter TL, Tsung A, Zahorchak AF, Nakao A, Nau GJ, Liew FY, Geller DA, Thomson AW. IL-1{beta}-driven ST2L expression promotes maturation resistance in rapamycin-conditioned dendritic cells. J Immunol. 2008 Jul 1;181(1):62-72. Robinson CM, Nau GJ. Interleukin-12 and Interleukin-27 regulate macrophage control of Mycobacterium tuberculosis. J Infect Dis. 2008 Jun 16. Kalivoda EJ, Stella NA, O'Dee DM, Nau GJ, Shanks RM. The cyclic AMP-dependent catabolite repression system of Serratia marcescens mediates biofilm formation through regulation of type 1 fimbriae. Appl Environ Microbiol. 2008 Jun;74(11):3461-70. Horzempa J, Tarwacki DM, Carlson PE Jr, Robinson CM, Nau GJ. Characterization and application of a glucose-repressible promoter in Francisella tularensis. Appl Environ Microbiol. 2008 Feb 1. Complete Publication Listing   Grant Support NIAID: Novel selectable markers for F. tularensis. Role: Principal Investigator NIAID: Host defenses and susceptibility to tuberculosis. Role: Principal Investigator NIAID: Host defenses and susceptibility to tuberculosis. Role: Principal Investigator   Other Links MMG Faculty Link CVR Webpage University of Pittsburgh

Gerard J. Nau, M.D., Ph.D. Office:  BSTWR E1256 Lab:BSTWR E1204 - 1206 Phone:412-383-8084 (E1204) Fax: 412-648-7772 (E1206) gjnau@pitt.edu   Academic Affiliations Assistant Professor Department of Microbiology and Molecular Genetics Assistant Professor Department of Medicine   Education 1983 B.S. Microbiology University of Notre Dame South Bend, IN 1988 Ph.D. Immunology University of Chicago Chicago, IL 1990 M.D. Pritzker School of Medicine University of Chicago Chicago, IL 1994 - 2000 Molecular Biology Whitehead Institute Cambridge, MA   Lab Personnel Postdoc: Joseph Horzempa, Ph.D. Research Technician: Dawn O'Dee Graduate Student: Paul Carlson