Publications: Erin Gaynor's Publications
Office #: 604-822-2710
History: B.A. (1990) and Ph.D. (1997), University of California San Diego; Postdoctoral, Stanford University (1998-2003)
Office: Room 2558, 2350 Health Sciences Mall, Life Sciences Centre
My research focuses on exploring the molecular mechanisms of pathogenesis in the foodborne human pathogen Campylobacter jejuni. C. jejuni is the leading worldwide cause of bacterial food poisoning; however, we know very little about how it causes disease, particularly in comparison to other pathogens such as E. coli and Salmonella.
C. jejuni interacts closely with intestinal epithelial cells during infection, causes marked inflammation, and the bacteria can both invade and translocate through the intestinal epithelium. One focus of my research is to identify and characterize C. jejuni genes involved in the intimate bacterium-host cell interaction, utilizing several new genomic and genetic tools developed in my laboratory. Using DNA microarrays, I identified several sets of C. jejuni genes whose expression was affected by close contact with human intestinal cells. We subsequently found that one of the up-regulated genes controls the C. jejuni stringent response, a general stress response that we found is required for C. jejuni to invade and survive inside epithelial cells. Ongoing projects are aimed at expanding our characterization of this new virulence determinant, exploring how the C. jejuni stringent response is regulated, and characterizing other bacterial factors that intersect with this response. Studies to explore other genes identified in the microarray screen are also planned.
We are also interested in understanding several specific regulatory elements that are likely to be involved in C. jejuni pathogenesis and colonization. We have already identified and characterized a novel two-component signal transduction system that appears to be specifically required for in vivo colonization; we are additionally exploring another two-component system that was up-regulated in the presence of host cells. Future work will focus on identifying the genes regulated by each of these systems and how they contribute to the bacteria’s ability to colonize and cause disease.
Finally, two longer-term goals of my research center on trying to understand how C. jejuni can live harmlessly as a commensal in most animal species yet causes severe disease in humans, and how a specific host or transmission environment contributes to pathogenicity. We have already determined that laboratory passage in a high O2 environment compromises the ability of C. jejuni to colonize its natural zoonotic hosts. Future work is aimed at (a) exploring how C. jejuni genotypes and genome evolution contribute to the successful colonization of specific host systems, and (b) investigating host cell responses to C. jejuni infection.