Author(s): Braden Warden, David Mefford
Mentor(s): Christopher Monson, Roger Gold
Institution SUU
This study investigated the timing of autoinducer release in relation to cell density for Pseudomonas aeruginosa, with a focus on elucidating quorum sensing mechanisms that drive virulence. An autoinducer is a signaling molecule released by bacteria to coordinate group behaviors, such as virulence, once a critical cell density is reached. Pseudomonas aeruginosa, the most common bacteria responsible for infections, is particularly known for its adaptability and pathogenicity in both clinical and environmental settings. Using the HPLC UV-vis, we analyzed cultured nutrient broth samples over a 48 hour period to chart the autoinducer release profile across different cell densities. Samples were consistently agitated to maximize growth while also limiting biofilm formation, filtered off, and extracted in preparation for analysis. A comparative approach with purchased standard chemicals were utilized to ensure accuracy in identifying the autoinducer, specifically N-butanoyl-L-homoserine lactone (C4-HSL). Under infectious conditions, this autoinducer influences the pathogen’s ability to cause apoptosis in host macrophages and neutrophils, resulting in cell death. Despite having a goal in quantifying these autoinducers over time, we were unsuccessful in determining autoinducers presence with an HPLC UV-vis process. Future research centered on determining virulence may utilize our processes with an edit towards the analytical detector instrument used. Literature theorizes the valuable insights into potential therapeutic interventions, enabling medical professionals to more effectively target Pseudomonas infections by blocking quorum sensing pathways. This research has the potential to address a critical gap by identifying the specific conditions under which Pseudomonas aeruginosa becomes virulent, offering new directions for future drug synthesis in bacterial infection management.