James Riordan
James Riordan
Assistant Professor
Contact
Office: BSF 217
Phone: 813/974-7457
Email:
Education
Ph.D. Molecular Biology, New Mexico State University, 2006.
Postdoctoral Fellow, Michigan State University.
Research
Molecular and physiological basis of bacterial pathogenesis and drug resistance.
Current research
The enterohemorrhagic Escherichia coli (EHEC) are a genetically heterogeneous group of bacterial pathogens, which have been linked to food- and water-borne outbreaks of enteric disease since the early 1980s. Central to EHEC transmission, is the ability to persist under extreme acid stress. This acid resistance (AR) represents a mechanism by which EHEC can subvert the disinfectant properties of gastric acid in the stomach, and is a determinant of low infectious dose. Using reverse genetics and DNA microarrays, we have recently determined that the E. coli alternative sigma factor N (rpoN), regulates the transcription of genes essential for full expression of the AR phenotype. One of the specific aims of our research, is to determine the mechanism by which rpoN regulates AR systems in EHEC, and the importance of rpoN in gastric passage. Understanding how AR is regulated is essential for the development of prevention/control strategies, aimed at reducing the transmission of EHEC, and other acid resistant enteric pathogens.
Shiga toxin is a central virulence determinant of EHEC, and is required for life-threatening sequelae, such as haemolytic uremic syndrome (HUS). Using quantitative real-time PCR and western blots, we have determined that an emergent subpopulation of EHEC O157:H7, associated with unusually high rates of HUS, is overproducing Shiga toxin. Moreover, we have shown that strains of this subpopulation are hypersensitive to DNA-damaging antibiotics (Cipro.) and antimicrobials (peroxide), which are known to enhance toxin production. A specific goal of this research, is to identify the genetic determinant(s) responsible for differences in basal and inducible Shiga toxin production. This information will help to delineate risk factors associated with specific genetic lineages of EHEC O157:H7.
Recent Publications
Riordan, J.T.*, and J.A. Tietjen. Sigma N (rpoN) commits enterohemorrhagic Escherichia coli (EHEC) to death by acid through repression of glutamate-dependent acid resistance. (Journal of Biological Chemistry, in review).
Riordan, J.T.*, C.W. Walsh, and T.S. Whittam. 2009. The sigma S (rpoS) and sigma N (rpoN) regulons of Escherichia coli O157:H7: contribution to virulence and stress resistance gene regulation. (BMC Genomics, in press).
Riordan, J.T., S.B. Viswanath, S.D. Manning, and T.S. Whittam*. 2008. Genetic differentiation of Escherichia coli O157:H7 clades associated with human disease by real-time PCR. Journal of Clinical Microbiology. 46(6): 2070.
Riordan, J.T., A. Muthaiyan, W. Van Voorhies, C.T. Price, J.E. Graham, B.J. Wilkinson, and J.E. Gustafson*. 2007. Response of Staphylococcus aureus to salicylate challenge. Journal of Bacteriology. 189(1): 220.
Delgado, A., J.T. Riordan, R. Lamichhane-Khadka, D.C. Winnett, J. Jimenez, K. Robinson, F.G. O’Brien, S.A. Cantore, and J.E. Gustafson*. 2007. Presence of a hetero-vancomycin-intermediate methicillin-resistant Staphylococcus aureus isolate from a medical center in Las Cruces, New Mexico. Journal of Clinical Microbiology. 45(4): 1325.
Riordan, J.T., J.O. O’Leary, and J.E. Gustafson. 2006. Contributions of sigB and sarA to distinct multiple antimicrobial resistance mechanisms of Staphylococcus aureus. International Journal of Antimicrobial Agents and Chemotherapy. 28(1): 54.