Seminars – Center for Microbial Dynamics and Infection

Upcoming schedule here. This trainee-run seminar series focused on new research in CMDI. It’s Fridays at 3pm and includes coffee and cookies. Fall 2025 seminars will be held in Cherry Emerson room 320.

Upcoming seminar:

Abstract:

Chronic respiratory polymicrobial infections are the major cause of loss of lung function in people with the genetic disorder, Cystic Fibrosis (CF). Staphylococcus aureus and Pseudomonas aeruginosa are the two most common pathogens infecting the airways of people with CF and are often found co-occurring as parts of larger polymicrobial communities. In CF airways and sputum samples, bacterial communities reside in spatially organized clusters of 10-104 cells referred to as aggregates. Several factors such as the abundance of host derived polymers like extracellular DNA (eDNA), mucin, and other bacterial cell surface properties regulate aggregate formation and assembly in CF airways. We previously found that P. aeruginosa cells that express O-specific antigen (OSA) form stacked aggregates in a synthetic CF sputum preclinical model containing eDNA and mucin (SCFM2). Building on these findings, we sought to investigate how interactions between P. aeruginosa and S. aureus shape the spatial organization of these two pathogens in CF airways. Using SCFM2 as infection model, we found that nuc1 -a highly efficient nuclease- produced by S. aureus, disrupts P. aeruginosa spatial organization and stacked aggregate assembly. We also demonstrated that nuc1 is expressed by S. aureus in the absences of P. aeruginosa andcan disrupt P. aeruginosa aggregates when no growing S. aureus cells are present. Our findings suggest that S. aureus Nuc1 production and activity is not dependent on P. aeruginosa presence and that S. aureus physiology can impact P. aeruginosa microbiogeography and physiology by altering the physiochemical properties of the environment. Our findings presented here, provide a foundation for furthering our understanding of interactions within microbial communities and the mechanisms that regulate microbial spatiotemporal dynamics and pathogenesis in chronic infections. Findings from this work provide a strong framework for leveraging these interspecific interactions to improve treatment outcomes and disease prevention by addressing microbial pathogenesis in chronic infections at the community scale.