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 gastric pathogen of humans that causes ulcers and gastric cancer in a small percentage of infected individuals.  Although the organism is capable of adhering to and even invading epithelial cells, a large percentage of the colonizing bacteria is found swimming in the mucous layer overlying the gastric epithelium.  The organism is likely to encounter very little host serum when residing near intact gastric tissue.  Our discovery of a chemically defined medium that supports consistent growth of H. pylori has opened several avenues of investigation previously out of reach to the field.  Culture of H. pylori in the absence of serum causes drastic changes in morphology, adherence, and motility compared to characteristics seen in the presence of serum.  Previously, all in vitro studies aimed at understanding colonization and pathogenesis were carried out in the presence of serum.  We are currently developing a model to study interactions between host cells and H. pylori in the absence of serum.  We are also working to identify the specific serum proteins responsible for triggering the observed phenotypic changes in H. pylori.  In parallel, we are also identifying H. pylori proteins/genes up- or down-regulated in the presence of serum by mass spectrometry and real-time PCR.  Several candidate genes have been identified and are being explored further.  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., 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. 

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.

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.