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Polymicrobial interactions between Staphylococcus aureus and Pseudomonas aeruginosa promote biofilm formation and persistence in chronic wound infections
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Polymicrobial interactions between Staphylococcus aureus and Pseudomonas aeruginosa promote biofilm formation and persistence in chronic wound infections
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Journal Article
Polymicrobial interactions between Staphylococcus aureus and Pseudomonas aeruginosa promote biofilm formation and persistence in chronic wound infections
2024
Overview
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.
Publisher
Cold Spring Harbor Laboratory Press,Cold Spring Harbor Laboratory
Subject
