Polymicrobial interactions between and promote biofilm formation and persistence in chronic wound infections.

Chronic, non-healing wounds are a leading cause of prolonged patient morbidity and mortality due to biofilm- associated, polymicrobial infections. and are the most frequently co-isolated pathogens from chronic wound infections. Competitive interactions between these pathogens contribute to enhanced virulence, persistence, and antimicrobial tolerance. utilizes the extracellular proteases LasB, LasA, and AprA to degrade surface structures, disrupt cellular physiology, and induce cell lysis, gaining a competitive advantage during co-infection. evades by employing aggregation mechanisms to form biofilms The cell wall protein SasG is implicated in biofilm formation by facilitating intercellular aggregation upon cleavage by an extracellular protease. We have previously shown that proteolysis by a host protease can induce aggregation. In this study, we report that proteases LasA, LasB, and AprA cleave SasG to induce aggregation. We demonstrate that SasG contributes to biofilm formation in response to interactions with proteases by quantifying aggregation, SasG degradation, and proteolytic kinetics. Additionally, we assess the role of SasG in influencing biofilm architecture during co-infection chronic wound co-infections. This work provides further knowledge of some of the principal interactions that contribute to persistence within chronic wounds co-infected with and their impact on healing and infection outcomes.