UC Irvine

Pseudomonas aeruginosa is an opportunistic pathogen that can move collectively on semi-solid surfaces through swarming motility, which gives rise to biofilms. The impact of diverse environmental factors on the organization of swarms is not well understood. We demonstrate that healthy P. aeruginosa swarming populations are re-directed by the Pseudomonas Quinolone Signal (PQS) quorum sensing molecule, which is over-produced by stressed P. aeruginosa infected with bacteriophage or treated with antibiotics. PQS has multiple functions, including serving as a quorum-sensing molecule, activating an oxidative stress response, and regulating the release of virulence and host-modifying factors. These mechanisms have the overall effect of limiting the threat of danger to a subpopulation, which promotes the survival of the overall population. Staphylococcus aureus, which is a natural competitor of P. aeruginosa, shows similar phenotype as stressed P. aeruginosa populations and repels P. aeruginosa swarms. This causes both bacterial species to remain spatially segregated and unmixed. The repulsion by S. aureus requires production of the small peptide phenol-soluble modulin (PSM), which is an amphipathic peptide that has surfactant properties owing to its large hydrophobic chains and hydrophilic side chains. We show that PSM fibrils produced by S. aureus mediate the repulsion of P. aeruginosa swarms. We determine that several long-chain amphipathic molecules with surfactant properties also repel P. aeruginosa swarms. Our results suggest a model in which surfactants can disrupt the surfactant layer produced by P. aeruginosa, causing reorganization of the swarming population. The segregation of P. aeruginosa and S. aureus via surfactant interactions promotes the survival of both species. This represents a general mechanism in which the organization of bacterial populations can be described by the interaction of the surfactants produced by the bacterial species. This observation has important implications for the formation and maintenance of bacterial populations in environments containing multiple species and on the outcomes of pathogenesis.