<p>Bacteria commonly protect themselves from a variety of threats by forming biofilms, which are communities of bacteria that are tightly packed together within an extracellular matrix. Biofilm formation has generally been thought to protect bacteria from phage infection. The opportunistic pathogen <i>Pseudomonas aeruginosa</i> produces biofilm matrices that can contain three distinct exopolysaccharides that contribute to the difficulty in treating infected patients. Here, we demonstrate that two diverse <i>P. aeruginosa</i> phages have evolved to exploit this biofilm matrix to access the bacterial cells by both binding to and degrading a major biofilm exopolysaccharide, Psl. We examined the effect of these phages on biofilms in different in vitro biofilm models and found that both phages prevent bacterial surface attachment, but only one of the two phages can disrupt a mature biofilm under flow. The phages also rapidly lead to the emergence of bacterial strains that produce reduced amounts of Psl and are unable to adhere to surfaces. These phages may be useful therapeutically by driving bacteria away from producing biofilms and shifting <i>P. aeruginosa</i> cells into the more treatable planktonic growth state.</p>

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Two unrelated Pseudomonas aeruginosa phages require the exopolysaccharide Psl for infection

  • Kristen Amyx-Sherer,
  • Leila C. Awasthi,
  • Amanda Zheng,
  • Anna Johannesman,
  • Michele LeRoux,
  • Courtney Reichhardt

摘要

Bacteria commonly protect themselves from a variety of threats by forming biofilms, which are communities of bacteria that are tightly packed together within an extracellular matrix. Biofilm formation has generally been thought to protect bacteria from phage infection. The opportunistic pathogen Pseudomonas aeruginosa produces biofilm matrices that can contain three distinct exopolysaccharides that contribute to the difficulty in treating infected patients. Here, we demonstrate that two diverse P. aeruginosa phages have evolved to exploit this biofilm matrix to access the bacterial cells by both binding to and degrading a major biofilm exopolysaccharide, Psl. We examined the effect of these phages on biofilms in different in vitro biofilm models and found that both phages prevent bacterial surface attachment, but only one of the two phages can disrupt a mature biofilm under flow. The phages also rapidly lead to the emergence of bacterial strains that produce reduced amounts of Psl and are unable to adhere to surfaces. These phages may be useful therapeutically by driving bacteria away from producing biofilms and shifting P. aeruginosa cells into the more treatable planktonic growth state.