Email: Office Phone: 318-675-8143
Laboratory Phone: 318-675-8146
Office Fax: 318-675-5764
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 mechanisms of pathogenesis
Helicobacter pylori is a very common gastric pathogen of humans that causes ulcers and gastric cancer in a small percentage of infected individuals. More recently, H. pylori has been linked to development of Parkinson’s disease. 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. In most cases, H. pylori maintains a delicate balance between persistence and pestilence; the bacterium obtains nutrients without causing severe damage to the host. My goal is to understand how this balance is achieved and how specific gene mutations affect colonization, host inflammatory response, and risk for Parkinson’s disease.
Adherence to host tissue is also critical for persistence of the organism. We have discovered that the H. pylori outer membrane proteins, AlpA and AlpB, bind to the host basement membrane protein, laminin. A strain lacking these proteins colonizes mice and gerbils at lower levels than the isogenic wild-type strain, but paradoxically causes increased inflammation in gerbils. Thus, we propose that specific interactions between H. pylori and the gastric epithelium serve to reduce the host inflammatory response.
We have developed a mouse parkinsonism model in collaboration with Dr. Michael Salvatore. The H. pylori mutant lacking AlpA and AlpB causes more rapid development of parkinsonian symptoms in this model. We are currently exploring the roles of inflammation and a putative neurotoxin in this disease model.
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, beta-cyclodextrin and an albumin-independent component in serum. J. Clin. Microbiol. 2001, 39(11):3842-50.
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.
Senkovich, O. , S. Ceaser, D. McGee, and T. L. Testerman. Unique host iron-utilization mechanisms of Helicobacter pylori revealed using iron-deficient chemically-defined media. 2010. Infection and Immunity. 78(5):1841-1849.
McGee, D. J., A. E. George, E. A Trainor, K. E. Horton, E. Hildebrandt, T. L. Testerman. Cholesterol enhances Helicobacter pylori resistance to antibiotics and LL-37. Antimicrob Agents Chemother. 2011 Apr 4. 55(6):2897-904. PMID: 21464244.
Senkovich, O. A., J. Yin, V. Ekshyyan, C. Conant, , J. Traylor, P. Adegboyega, D.J. McGee, R.E. Rhoads, S. Slepenkov and, T.L. Testerman. H. pylori AlpA and AlpB bind host laminin and influence gastric inflammation in gerbils. 2011. Infection and Immunity. 79(8):3106-16. PMID: 21576328.
All Publications: PubMed