Timothy R. Billiar, Professor
MD, University of Chicago
Email:
billiartr@upmc.edu
Dr. Billiar is Professor and Chair of the Department of Surgery. His laboratory has had a long standing interest in the mechanisms involved in acute cellular and organ injury in inflammatory states such as shock, trauma, and sepsis. His laboratory focuses research in two main areas. First, his laboratory investigates the mechanisms leading activation of inflammation following acute cellular and organ damage. There is a special emphasis on danger associated molecular pattern molecules and pattern recognition receptors in this response. Model systems include organ ischemia and reperfusion as well as systemic insult such as shock and tissue trauma. Analysis includes markers of inflammation, the immunological consequences, mechanisms of organ injury and genome wide studies.
The second area of investigation includes examining pathways leading to cell death in hepatocytes. This work stems from a long standing interest in the actions of nitric oxide in the liver and has lead to an interest in understanding how cells such as hepatocytes regulate the response to both protective and damaging stimuli. The work involves both invitro and invivo systems.
The goal of the research in both areas is to define mechanisms and identify therapeutic targets.
Recent Publication
Tsung, A, Sahai, R, Tanaka H, Nakao A, Fink MP, Lotze MT, Yang H, Li J, Tracey KJ, Geller DA, Billiar TR. The nuclear factor HMGB1 mediates hepatic injury after murine liver ischemia reperfusion. J Exp Med. 2005 April 4; 201(7):1135-1143.
Loughran PA, Stolz DB, Vodovotz Y, Watkins SC, Simmons RL, Billiar TR. Monomeric iNOS synthase localizes to peroxisomes in hepatocytes. Proc. Natl. Acad. Sci. USA 2005; 102: 13837-13842.
Izuishi K, Tsung A, Jeyabalan G, Critchlow ND, Li J, Tracey KJ, Fink MP, Geller DA, Billiar TR. Cutting edge: High-mobility group box 1 preconditioning protects against liver ischemia-reperfusion injury. Journal of Immunology 2006, 176:7154-7158.
Levy RM, Prince JM, Yang R, Mollen KP, Liao H, Watson GA, Fink MP, Vodovotz Y, Billiar TR. Systemic inflammation and remote organ damage following bilateral femur fracture requires toll-like receptor 4. Am J Physiol Regulatory Integrative Comp Physiol 2006, 291:970-976.
Tsung A, Klune JR, Jeyabalan G, Cao Z, Peng X, Stolz DB, Geller DA, Rosengart MR, Billiar TR. Ischemia-induced HMGB1 release by hepatocytes involves toll-like receptor 4 dependent reactive oxygen species production and calcium mediated signaling. Journal of Experimental Medicine. (In Press)
