Ken Barth Ph.D.
Address: Boston University Department of Medicine, Section of Infectious Diseases. 650 Albany st. X-620. Boston, MA 02118
I have been transformed into a diehard Bills and Sabres fan as a result of being a proud Buffalo, New York native. I have a large family, most of which have remained in the western New York area. I love activities within the outdoors, whether its fishing, camping, boating, or sports. I recently completed my graduate degree in Microbiology from the University of Rochester: School of Medicine. My doctoral research focused on reactive nitrogen species and Neisseria gonorrhoeae, the causative agent of the sexually transmitted disease gonorrhea. Studies examined the metabolism of nitric oxide by Neisseria gonorrhoeae and other commensal Neisseria species. In addition, we discovered very high level resistance of the gonococcus to another reactive nitrogen species, peroxynitrite, commonly produced within immune cells as a mechanism of intracellular killing. I recently moved to Boston to join the Genco laboratory at Boston University Medical Center in order to begin work on another Gram-negative bacterial species, Porphyromonas gingivalis.
Postdoctoral Fellow, Boston University School of Medicine, Department of Medicine; Boston, MA
Ph.D Microbiology, University of Rochester: School of Medicine and Dentistry; Rochester, NY
M.S. Microbiology, University of Rochester: School of Medicine and Dentistry; Rochester, NY
B.S. Biology, Niagara University; NY
I am most interested within the interface between pathogen and host, in context of innate immunity. Often researchers study the symptoms within a host during a specific disease, yet the interactions of how a pathogen is able to subvert, avoid, or overcome the normal functioning of the immune response is overlooked. These evolved mechanisms highlight the complexities of bacterial virulence. Current research involves P. gingivalis, a pathogen that has been linked to periodontal disease and atherosclerosis. During P. gingivalis infection there is an increase in local inflammation, cytokine/chemokine production levels, as well as Toll-like receptor expression. In order to study the effects of bacterial infection in context of atherosclerosis, we utilize primary endothelial cells. These serve as a model for not only proper activation of the innate immune response, but also deciphering any alteration to the normal signaling pathways as a result of bacterial intervention.
Barth, K., Isabella, V., and V. L. Clark.
Biochemical and genomic analysis of the denitrification pathway within the Neisseria genus. Microbiol. Accepted August, 2009.
Barth, K., Isabella, V., Wright, L., and V. L. Clark.
Resistance to reactive nitrogen species in Neisseria gonorrhoeae.2009. Microbiol 155: 2532-2545.
Barth, K. & V. L. Clark.
Differences in nitric oxide steady states between arginine, hypoxanthine, uracil auxotrophs (AHU) and non-AHU strains of Neisseria gonorrhoeae during anaerobic respiration in the presence of nitrite. 2008. Can J Microbiol 54: 639-646
Isabella, V., Wright, L., Barth, K., Spence, J. M., Grogan, S., Genco, C. A., and V. L. Clark.
cis- and trans-acting elements involved in regulation of norB (norZ), the gene encoding nitric oxide reductase in Neisseria gonorrhoeae. 2008. Microbiology. 154: 226-239.
Clark, V. L., Isabella, V. M., Barth, K., and T. Overton. 2008.
Regulation and function of the Neisserial denitrification pathway: life with limited oxygen. Caroline Genco and Lee Wetzler, editors. Neisseria: Molecular Mechanisms of Pathogenesis. Horizon Scientific Press, Norwich, UK., In press.