Associate Professor

Contact Information:
Email: dmcgee@lsuhsc.edu
Office Phone: 318-675-8138
Laboratory Phone: 318-675-8139
Office Fax: 318-675-5764

Education/Training:
Postdoctoral Study, University of Maryland-Baltimore
Ph.D., Microbiology and Immunology, 1997, Allegheny University of the Health Sciences (now Drexel University)
B.S., Microbiology, 1992, Philadelphia College of Pharmacy and Science (now University of the Sciences in Philadelphia)

Major Research Interests:  Helicobacter pylori and Arcanobacterium haemolyticum host-pathogen interactions

Helicobacter pylori is a fascinating bacterium that spends most of its time in the harsh acidic environment of the human stomach.  A very successful and highly-adapted pathogen, H. pylori infects about 50% of the world's population, causing an extraordinary range of disease severity-- from gastritis and peptic ulcers to gastric cancer and MALT lymphoma. H. pylori thus serves as a model for pathogen-induced carcinogenesis.  Disease severity is dependent on genes produced by the bacterium, genetic polymorphisms of the host, and environmental influences (eg., diet), making this organism an exciting challenge to unravel these various contributors to disease processes.   Our long-term goal is to unravel the mechanisms by which H. pylori causes these diverse disease manifestations.  Our recent interest has centered on understanding the role of the chemotaxis genes, and the enzymes arginase and serine deaminase in pathogenesis.  We are also examining the role of host cholesterol in H. pylori colonization.  Our research may lead to novel insights into host-pathogen interactions and aid in development of a desperately needed vaccine to prevent H. pylori infection and its sequelae.

Arcanobacterium haemolyticum is a Gram positive rod that is an emerging pathogen.  It causes pharyngitis in adolescents and wound infections.  Our understanding of this organism’s physiology, metabolism and virulence are almost completely unknown.  Several recently initiated projects include random sequence analysis of the genome, proteomics of organisms grown under different conditions, and establishment of a tissue culture model.  We will focus on characterizing genes and proteins that help us to understand the mechanisms of pathogenesis.

Representative publications:

McGee, D. J.*, M. L. Langford, E. L. Watson, J. E. Carter, Y.-T. Chen and K. M. Ottemann*.  2005.  Colonization and inflammation deficiencies in Mongolian gerbils infected with Helicobacter pylori chemotaxis mutants.  Infect. Immun., 73: 1820-1827.  * Co-corresponding authors. 

McGee, D. J., S. Kumar, R. J. Viator, J. R. Bolland, D. Spadafora, T. L. Testerman, J. Ruiz, D. J. Kelly, L. K. Pannell, and H. J. Windle.  2006.  Helicobacter pylori thioredoxin is an arginase chaperone and guardian against oxidative and nitrosative stresses.  J. Biol. Chem., 281:3290-3296.

Testerman, T. L., P. B. Conn, H. L. T. Mobley, and D. J. McGee.  2006.  Nutritional requirements and antibiotic resistance patterns of Helicobacter species in chemically-defined media.  J. Clin. Microbiol., 44: 1650-1658.

Langford, M. L., J. Zabaleta, T. L. Testerman, A. Ochoa, and D. J. McGee.  2006.  In vitro and in vivo complementation of the Helicobacter pylori arginase mutant using an intergenic chromosomal site. Helicobacter, 11:477-493.

Hovey, J. G., E. L. Watson, M. L. Langford, E. Hildebrandt, S. Bathala, J. R. Bolland, D. Spadafora, G. L. Mendz, and D. J. McGee.  2007.  Genetic microheterogeneity and phenotypic variation of Helicobacter pylori arginase in clinical isolates.  BMC Microbiol. 7:26 (http://www.biomedcentral.com/1471-2180/7/26).

Williams, S. M., Y.-T. Chen, T. Anderman, J. E. Carter, D. J. McGee and K. M. Ottemann.  2007.  Helicobacter pylori chemotaxis modulates inflammation and gastric epithelium interactions in infected mice.  Infect. Immun. 75: 3747-3757.