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Calcium Regulation of Virulence in Pseudomonas Aeruginosa

Undergraduate #125
Discipline: Biological Sciences
Subcategory: Microbiology/Immunology/Virology
Session: 2
Room: Exhibit Hall A

Jacee L. McCoy - Oklahoma State University
Co-Author(s): Leah A. Kafer, Oklahoma State University, Stillwater, OK; Biraj B. Kayastha, Oklahoma State University, Stillwater, OK; Marianna A. Patrauchan,Oklahoma State University, Stillwater,OK



Pseudomonas aeruginosa is an opportunistic pathogen that causes severe chronic infections in the lungs of Cystic Fibrosis (CF) patients, were elevated levels of calcium (Ca2+) are commonly detected. Our group has discovered that elevated Ca2+ enhances the production of several virulence factors in P. aeruginosa. Therefore, we hypothesized that elevated Ca2+ also enhances the ability of the pathogen to cause disease in an animal host as we earlier showed in plants. Further, this study aimed to determine the role of EfhP in Ca2+-regulated virulence of P. aeruginosa. EfhP is a Ca2+-binding protein, which has been shown to mediate Ca2+-regulation of several virulence factors as well as resistance to oxidative stress. To test this hypothesis and define the role of EfhP in Ca2+-dependent virulence of this pathogen, we used Galleria mellonella wax worm as an animal model. We injected the wax worms with the wild type and EfhP deletion mutant, monitored the death and determined the pathogen?s LD50. We also assessed the transcriptional regulation of EfhP in response to Ca2+ using EfhP promoter genetic construct in a promoter activity assay. So far, we showed that the mutant lacking EfhP gene exhibited a significantly lower virulence than the wild type when grown at elevated Ca2+. Additionally, we have found an increased transcriptional response of EfhP in the presence of Ca2+. This research provides insight into the Ca2+ regulatory system controlling virulence and pathogenic interactions within a host. This knowledge is essential for future development of strategies and approaches for preventing or controlling P. aeruginosa infections.

Funder Acknowledgement(s): I thank Dr. Marriette Barbier, West Virginia University, for guidance in this study. Additionally, I am thankful for funding provided by NIH COBRE, NIH Diversity Supplement and Oklahoma Louis Stokes Alliance for Minority Participation

Faculty Advisor: Marianna Patrauchan, m.patrauchan@okstate.edu

Role: I conducted all parts of the research outlined in the abstract.

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This material is based upon work supported by the National Science Foundation (NSF) under Grant No. DUE-1930047. Any opinions, findings, interpretations, conclusions or recommendations expressed in this material are those of its authors and do not represent the views of the AAAS Board of Directors, the Council of AAAS, AAAS’ membership or the National Science Foundation.

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