ABS 002: Oxidative Stress Response: Induced Antimicrobial Resistance in Pseudomonas aeruginosa

Charles Heinz ¹, Max Peng ¹, Dr. Anuradha Goswami ¹

¹ Department of Biological Sciences, University of Notre Dame

Van Wickle (2026) Volume 2, ABS002

Introduction: Reactive oxygen species (ROS) are unavoidable byproducts of aerobic metabolism and accumulate during host immune responses, creating oxidative stress that can reshape bacterial physiology and antimicrobial susceptibility. Pseudomonas aeruginosa, an opportunistic Gram-negative pathogen, is a leading cause of ventilator-associated pneumonia, burn wound infections, and chronic lung colonization in patients with cystic fibrosis. Its intrinsic and adaptive resistance mechanisms make treatment challenging, particularly under inflammatory conditions, where reactive oxygen species are abundant. This study investigated how acute and prolonged oxidative stress influence physiological and phenotypic responses in P. aeruginosa.

Methods: Mid-log phase cultures were exposed to graded concentrations of hydrogen peroxide (H₂O₂), with sampling at T = 0 (pre-treatment), T = 0.5 (30 minutes post-exposure), and T = 24 (24 hours post-exposure). Optical density (OD600) measurements, siderophore quantification using the Chrome Azurol S assay, and subsequent minimum inhibitory concentration (MIC) analyses were performed in accordance with standardized recovery procedures.

Results: Preliminary findings indicate that ROS accumulation did not follow zero-order kinetics under oxidative stress, suggesting dynamic regulation of ROS generation and scavenging pathways rather than a constant rate of formation. Notably, siderophore production increased significantly after 24 hours of exposure. This delayed elevation suggests an adaptive iron-acquisition response under oxidative stress, potentially linked to iron homeostasis, redox balance, and protection against Fenton chemistry-mediated damage.

Discussion: These findings support a model in which oxidative stress triggers temporally distinct physiological adjustments in P. aeruginosa, including altered redox dynamics and enhanced siderophore-mediated iron scavenging. Ongoing MIC analyses will determine whether oxidative stress-induced siderophore upregulation correlates with altered antibiotic susceptibility. Given the prevalence of oxidative stress within infected host tissues, understanding these adaptive mechanisms may clarify how inflammatory microenvironments influence antimicrobial resistance and persistence in clinical settings.