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 Research Assistant Professor
Contact Information:
Email: tteste@lsuhsc.edu
Office Phone: 318-675-8143
Laboratory Phone: 318-675-8146
Office Fax: 318-675-5764
Education/Training:
Postdoctoral Study, University of Maryland, University of South Alabama
Ph.D., Microbiology and Immunology, 1999, University of Colorado Health Sciences Center
B.S., Biochemistry, 1991, University of Minnesota
Major Research Interests: Helicobacter pylori physiology and pathogenesis
Helicobacter pylori is a very common gastric pathogen of humans that causes ulcers and gastric cancer in a small percentage of infected individuals. The organism is found swimming in the mucous layer overlying the gastric epithelium and within gastric pits, with a subpopulation found adhering to and even invading epithelial cells. The organism is likely to encounter very little host serum when residing near intact gastric tissue, but would encounter serum near an ulcer. Since H. pylori relies on the host for survival and rarely causes fatal perforated ulcers, the organism may modulate virulence properties in order to limit damage. We hypothesize that serum signals tissue damage and alters both H. pylori gene expression and adherence properties. Our discovery of a serum-free, chemically-defined medium that supports consistent growth of H. pylori has opened several avenues of investigation previously out of reach to the field. We have used microarray and proteomic analysis to identify H. pylori genes/proteins up- or down-regulated in the presence of serum. Several candidate genes have been identified and are being explored further. The list includes several putative adhesins, a putative protease, and genes involved in iron metabolism. One putative adhesin appears to mediate adherence to a host basement membrane protein. A strain lacking this gene colonizes mice and gerbils at lower levels than the isogenic wild-type strain, but paradoxically causes increased inflammation in gerbils. Thus, this gene could represent an “antivirulence” factor.
Availability of chemically-defined media has also allowed us to explore H. pylori utilization of host iron-binding molecules. Free iron is likely to be abundant in gastric juice, but extremely scarce within gastric crypts and intracellularly. Wresting iron from host iron-binding molecules may therefore be important for persistent colonization. Although H. pylori is able to use certain host iron sources, its acquisition mechanisms appear to differ substantially from those of other bacterial pathogens. The results of these studies may offer significant insights into the host-pathogen interactions that result in lifelong colonization by H. pylori.
Representative Publications:
Testerman, T. L., D. J. McGee, and H. L. T. Mobley. Chapter 34: Adherence and Colonization. In Helicobacter pylori: Physiology and Genetics. 2001. pp. 381-417. ASM Press, Washington, D. C.. Mobley, H. L. T, G. L. Mendz, and S. L. Hazell, eds.
Testerman, T. L., McGee, D. J., and H. L. T. Mobley. Growth of Helicobacter pylori in the chemically-defined medium, Ham's F-12, requires zinc, hypoxanthine and pyruvate, and is enhanced by cholesterol, b-cyclodextrin and an albumin-independent component in serum. J. Clin. Microbiol. 2001, 39(11):3842-50.
McGee, D. J., Coker, C., Testerman, T. L., Harro, J. M., Gibson, S. V., Mobley, H. L. T. The Helicobacter pylori flbA flagellar biosynthesis and regulatory gene is required for motility and virulence and modulates urease of H. pylori and Proteus mirabilis. 2002. J. Medical Microbiol., 51(11):958-70.
McGee, D. J., Zabaleta, J., Viator, R., Testerman, T. L., Ochoa, A., Mendz, G. Purification and characterization of Helicobacter pylori arginase, RocF: unique features among the arginase superfamily. 2004. Eur. J. Biochem. 271(10):1952-62.
McGee, D. J., Kumar, S., Viator, R. J. Bolland, J. R., Ruiz, J., Spadafora, D., Testerman, T. L., Kelly, D. J., Pannell, L. K., and H. J. Windle. Helicobacter pylori Thioredoxin is and Arginase Chaperone and Guardian Against Oxidative and Nitrosative Stresses. 2005. J. Biol. Chem. 281(6): 3290-3296.
Langford, M. L., J. Zabaleta, T. L. Testerman, A. Ochoa, and D. J. McGee. Development of a novel system to complement genes into the chromosome of Helicobacter pylori without disruption of known open-reading frames: Complementation of the arginase mutant. 2006. Helicobacter. 11(5):477-93.
Testerman, T. L., Conn, P. B., Mobley, H. L. T., and D. J. McGee. Nutritional Requirements and Antibiotic Resistance Patterns of Helicobacter Species in Chemically-Defined Media. 2006. J. Clin. Microbiol. 44(5): 1650-1658.
Williams, J. C., K. A. McInnis, and T. L. Testerman. Adherence of Helicobacter pylori to abiotic surfaces is influenced by serum. 2008. Appl Environ Microbiol. 74(4):1255-1258.
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