B.S., Indiana University of Pennsylvania
M.S., Indiana University of Pennsylvania
Ph.D., University of Kentucky
My research interests have always centered on bacterial pathogenesis. I completed my M.S. degree at Indiana University of Pennsylvania studying Legionella pneumophila, the causative agent of Legionnaires’ Disease, and earned my Ph.D. at the University of Kentucky while studying Campylobacter jejuni and Helicobacter pylori, which cause food-borne gastroenteritis and stomach inflammation/ulcers, respectively. As a postdoctoral fellow at the University of Rochester, I began studying Pseudomonas aeruginosa, a Gram negative bacterium that is one of the leading sources of infections acquired by hospitalized patients, causing ailments such as pneumonia, and urinary tract and surgical wound infections. P. aeruginosa also infects most cystic fibrosis patients at a very early age and causes a chronic pneumonia that is virtually impossible to cure. In addition, this opportunistic pathogen is a regular source of corneal keratitis in contact lens wearers, with serious infections leading to blindness. Our research on P. aeruginosa is focused on how this pathogen controls its virulence through cell to cell signals. P. aeruginosa uses at least three small chemicals to communicate intracellularly and regulate a large number of virulence factors and other cellular functions. This regulation is dependent on the density of the bacterial cells and in this manner, P. aeruginosa monitors and responds to its own population. We speculate that P. aeruginosa benefits from this regulation by delaying virulence factor expression until enough bacteria are present to overcome the immune response that will be elicited by the presence of certain virulence factors. My laboratory has identified a novel intracellular signal, 2-heptyl-3-hydroxy-4-quinolone, and refer to it as the Pseudomonas Quinolone Signal (PQS). This signal controls numerous virulence factors and is required for P. aeruginosa to cause infections in plants, insects, and animals. We have also directly found this signal in the sputum of cystic fibrosis patients, which suggests that it plays a role in chronic lung infections. Our studies have focused on understanding the synthesis of PQS and how this synthesis is regulated. We have discovered that at least 5 operons are involved in PQS synthesis and have undertaken studies to identify key enzymes involved in PQS synthesis. We are also examining the activity of PQS and how it regulates genes which it controls. Our long term goal is to identify aspects of PQS-signaling that can be exploited for drug targeting. While such targets would probably not produce a bactericidal compound, they could produce a therapeutic agent that will disrupt the PQS signaling cascade and thereby lessen the virulence of P. aeruginosa. Such compounds could augment known antibiotics or make the bacterium more susceptible to clearance by the host immune system.
If you are interested in joining our laboratory or have any questions for me, please contact me at 252-744-2351 or email@example.com.
Pesci, E.C., and B.H. Iglewski. 1999. Signalling in Pseudomonas aeruginosa. Pp. 105-115 in Microbial Signalling and Communication. Cambridge University Press, Cambridge, UK.
Pesci, E.C., J. Milbank, J.P. Pearson, S.L. McKnight, A.S. Kende, E.P. Greenberg, and B.H. Iglewski. 1999. Quinolone signaling in the cell-to-cell communication system of Pseudomonas aeruginosa. Proc. Natl. Acad. Sci. USA 96:11229-11234.
Pesci, E. C. 2000. New signal molecules on the quorum-sensing block: response. Trends in Micro. 8:103-104.
McKnight, S.L., B.H. Iglewski, and E.C. Pesci. 2000. The Pseudomonas quinolone signal (PQS) regulates rhl quorum sensing in Pseudomonas aeruginosa. J. Bacteriol. 182: 2702-2708.
Branny, P., J.P. Pearson, E.C. Pesci, T. Kohler, B.H. Iglewski, and C. Van Delden. 2001. Inhibition of quorum sensing by a Pseudomonas aeruginosa dksA homologue. J. Bacteriol. 183:1531-1539.
Calfee, M.W., J.P. Coleman, and E.C. Pesci. 2001. Interference with Pseudomonas Quinolone Signal synthesis inhibits virulence factor expression by Pseudomonas aeruginosa. Proc. Natl. Acad. Sci. USA 98:11633-11637.
de Kievit , T. R., Y. Kakai, J. K. Register, E. C. Pesci, and B. H. Iglewski. 2002. Role of the Pseudomonas aeruginosa las and rhl quorum-sensing systems in rhlI regulation. FEMS Microbiol Lett. 212:101-106.
Gallagher, L. A., S. L. McKnight, M. Kuznetsova, E. C. Pesci, and C. Manoil. 2002. Functions required for extracellular quinolone signaling by Pseudomonas aeruginosa. J. Bacteriol. 184:6472-6480.
D'Argenio, D. A., M. W. Calfee, P. B. Rainey, and E. C. Pesci. 2002. Autolysis and autoaggregation in Pseudomonas aeruginosa colony morphology mutants. J. Bacteriol. 184:6481-6489.
Collier, D. N., L. Anderson, S. L. McKnight, T. L. Noah, M. Knowles, R. Boucher, U. Schwab, P. Gilligan, and E. C. Pesci. 2002. A bacterial cell to cell signal in the lungs of cystic fibrosis patients. FEMS Microbiol. Lett. 215:41-46.
Pesci, E.C., and B.H. Iglewski. 2003. Quorum Sensing. p. 55-65, in Bacterial Protein Toxins. Amer. Soc. for Microbiology Press., Washington, DC.
McGrath, S., Wade, D. S., and E. C. Pesci. 2004. Dueling Quorum Sensing Systems in Pseudomonas aeruginosa Control the Production of the Pseudomonas Quinolone Signal (PQS). FEMS Microbiol. Lett. 230:27-34.
Erickson, D. L., J. L. Lines, E. C. Pesci, V. Venturi, and D. G. Storey. 2004. Pseudomonas aeruginosa relA Contributes to Virulence in Drosophila melanogaster. Infect. Immun. 72:5638-5645.
Calfee, M. W., J. G. Shelton, J. A. McCubrey, and E. C. Pesci. 2005. Solubility and bioactivity of the Pseudomonas Quinolone Signal (PQS) are increased by a Pseudomonas aeruginosa-produced surfactant. Infect. Immun. 73:878-882.
Wade, D. S., M. W. Calfee, E. R. Rocha, E. A. Ling, E. Engstrom, J. P. Coleman, and E. C. Pesci. 2005. Regulation of PQS synthesis in Pseudomonas aeruginosa. J. Bacteriol. 187:4372-4380.
Carty, N. L., N. Layland, J. A. Colmer-Hamood, M. W. Calfee, E. C. Pesci, A. N. Hamood. 2006. PtxR modulates the expression of QS-controlled virulence factors in the Pseudomonas aeruginosa strain PAO1. Molecular Microbiology. 61:782-794.
Farrow, J. M., and E. C. Pesci. 2007. Two Distinct Pathways Supply Anthranilate as aPrecursor of the Pseudomonas Quinolone Signal. J. Bacteriol. 189:3425-3433.
Cugini, C., M. W. Calfee, J. M. Farrow, D. K. Morales, E. C. Pesci, and D. A. Hogan. 2007 Farnesol, a common sesquiterpene, inhibits PQS production in Pseudomonas aeruginosa. Mol. Microbiol. 65:896-906.
Coleman, J. P. L.L. Hudson, S. L. McKnight, J. M. Farrow, M. W. Calfee, C. A.Lindsey, and E. C. Pesci. 2008. Pseudomonas aeruginosa PqsA is an anthranilate-coenzyme A ligase. J. Bacteriol. 190:1247-1255.
Oglesby, A. G., J. M. Farrow, J. H. Lee, A. P. Tomaras, E. P. Greenberg, E. C. Pesci, and M. L. Vasil. 2008. The influence of iron on Pseudomonas aeruginosa physiology: a regulatory link between iron and quorum sensing. J. Biol. Chem. 283:15558-15567.
Rajamani, S., W. D. Bauer, J. B. Robinson, J. M. Farrow, E. C. Pesci, M. Teplitski, M. Gao, R. T. Sayre, and D. A. Phillips. 2008. The vitamin riboflavin and its derivative lumichrome activate the LasR bacterial quorum sensing receptor. Mol. Plant-Microbe Interactions. 21:1184-1192.
Farrow, J. M., Z. M. Sund, M. L. Ellison, D. S. Wade, J. P. Coleman, and E. C. Pesci. 2008. PqsE Functions Independently of PqsR-Pseudomonas Quinolone Signal and Enhances the rhl Quorum-Sensing System. J. Bacteriol. 190:7043-7051.
Ling, E. A., M. Ellison, and E. C. Pesci. 2009. The Development of a Broad SpecificityAutoinducer Bioassay. Plasmid. 62:16-21.
Bera, A.K., V. Atanasova, H. Robinson, E. Eisenstein, J.P. Coleman, E.C. Pesci, J.F. Parsons. 2009. Structure of PqsD, a Pseudomonas quinolone signal biosynthetic enzyme, in complex with anthranilate. Biochem. 48:8644-8655.
Knoten, C. A., L. L. Hudson, J. P. Coleman, J. M. Farrow, and E. C. Pesci. 2011. KynR, a Lrp/Asn-type Transcriptional Regulator, directly Controls the Kynurenine Pathway in Pseudomonas aeruginosa. J. Bacteriol. 193:6567-6575.