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Brad Cookson
Professor of Microbiology and Laboratory Medicine

Email: cookson@u.washington.edu
Phone: (206) 598-6131
Office Location: Health Sciences J-237A
Campus Box: 357735







Dr. Brad Cookson received a B.S. degree from the University of Utah, where he worked on genetic regulation of NAD metabolism in Salmonella typhimurium with Dr. John Roth. He purified and defined the molecular structure of the Bordetella pertussis tracheal cytotoxin to earn his Ph.D. at Washington University in the lab of Dr. William Goldman. He also received a M.D. from Washington University, was awarded an Olin Medical Fellow, and received the Alexander Berg Award in Microbiology and Immunology. After completing residency training in Clinical Pathology at the University of Washington, his post-doctoral studies on cellular immune responses to microbial pathogens were conducted in the laboratory of Dr. Michael Bevan, also at the University of Washington. In addition to an appointment in the Department of Microbiology, Dr. Cookson is a Professor in the Department of Laboratory Medicine, Head of the Clinical Microbiology Division, and Director of the Microbiology section of Molecular Diagnosis. He received a Pfizer New Faculty Scholar award and chaired the FASEB Summer Research Conference, Microbial Pathogenesis: Mechanisms of Infectious Diseases.

Research in Dr. Cookson's lab revolves around the idea that a greater understanding of immune responses will provide novel insights into host-pathogen interactions. This information will help us develop effective tools for diagnosing infectious diseases and help us design therapeutic strategies that favor quality outcomes for infected hosts. Salmonella and Yersinia infections cause both systemic and localized diseases, and studying these systems provides an excellent opportunity to understand: 1) the mechanisms of protective immunity conferred by novel immunization strategies; 2) how virulent bacteria escape primary immune responses and cause sepsis; 3) the contributions of innate immune functions to the development of immunity; and 4) the role of T cell-macrophage interactions in combating infections caused by pathogens like Salmonella, the Mycobacteria, and Leishmania. In the course of these studies, the Cookson lab uses techniques in cellular immunology, bacterial genetics, biochemistry, and molecular biology.

We also partner with engineers and private industry to utilize and develop biotechnology in two areas. First, to define the mechanism of proinflammatory programmed eukaryotic cell death called pyroptosis (to distinguish it from noninflammatory apoptosis) induced by certain bacterial infections. The pyroptosis pathway has broad implications for a variety of biological systems, including the immune, cardiovascular, and central nervous systems. The goal is to better understand organ damage resulting from infections, cancer, heart attacks, and strokes. Second, to utilize powerful amplification and detection systems to diagnose bacterial and fungal infections. The goal is to improve the medical management of hospitalized patients suffering from infectious diseases.

Selected Publications:

Fink, S. L., T. L. Bergsbaken, and B. T. Cookson. 2008. Anthrax lethal toxin and Salmonella elicit the common cell death pathway of caspase-1-dependent pyroptosis via distinct mechanisms. Proc. Natl. Acad. Sci. USA. 105(11):4312-7.

Alaniz, R. C., B. L. Deatherage, J. Cano Lara, and B. T. Cookson. 2007. Membrane vesicles are immunogenic facsimiles of Salmonella typhimurium that potently activate dendritic cells, prime protective B- and T-cell responses, and stimulate protective immunity in vivo. J. Immunol. 179: 7692-7701.

Bergsbaken, T. L., and B. T. Cookson. 2007. Macrophage activation redirects Yersinia-infected host cell death from apoptosis to Caspase-1-dependent pyroptosis. PLoS Pathogens. 3(11): e161 Fink, S. L., and B. T. Cookson. Pyroptosis and host cell death responses to Salmonella infection. 2007. Cell Microbiol. 9(11): 2562-70.

Fink, S. L. and B. T. Cookson. 2006. Caspase-1-dependent pore formation during pyroptosis leads to osmotic lysis of infected host macrophages. Cell Microbiol. 8(11): 1812-1825.

Alaniz, R. A., L. A. Cummings, M. A. Bergman, S. L. Rassoulian-Barrett and B. T. Cookson. 2006. Salmonella typhimurium coordinately regulates FliC location and reduces dendritic cell activation and antigen presentation to CD4+ T cells. J. Immunol. 177: 3983-3993.

Cummings, L. A., W. D. Wilkerson, T. L. Bergsbaken, and B. T. Cookson. 2006. In vivo, fliC expression by Salmonella enterica serovar Typhimurium is heterogeneous, regulated by ClpX, and anatomically restricted. Mol. Microbiol. 61(3): 795-809.





Department of Microbiology · University of Washington · Box 357735 · Seattle WA 98195-7735

phone: (206) 543-5824 · fax: (206) 543-8297 · micro@u.washington.edu