Albumin Inhibits Pseudomonas aeruginosa Quorum Sensing and Alters Polymicrobial Interactions
Abstract
Polymicrobial interactions are complex and can influence the course of an infection, as is the case when two or more species exhibit a synergism that produces a disease state not seen with any of the individual species alone. Cell-to-cell signaling is key to many of these interactions, but little is understood about how the host environment influences polymicrobial interactions or signaling between bacteria. Chronic wounds are typically polymicrobial, with Staphylococcus aureus and Pseudomonas aeruginosa being the two most commonly isolated species. While P. aeruginosa readily kills S. aureus in vitro , the two species can coexist for long periods together in chronic wound infections. In this study, we investigated the ability of components of the wound environment to modulate interactions between P. aeruginosa and S. aureus . We demonstrate that P. aeruginosa quorum sensing is inhibited by physiological levels of serum albumin, which appears to bind and sequester some homoserine lactone quorum signals, resulting in the inability of P. aeruginosa to produce virulence factors that kill S. aureus . These data could provide important clues regarding the virulence of P. aeruginosa in albumin-depleted versus albumin-rich infection sites and an understanding of the nature of friendly versus antagonistic interactions between P. aeruginosa and S. aureus .
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Sep 01, 2017
- Source ID
- 10.1128/iai.00116-17
Entities
People
- Aimee K. Wessel
- Allie Clinton Smith
- Anne Rice
- Bryan Sutton
- Kendra P. Rumbaugh
- Marvin Whiteley
- Rebecca Gabrilska
Organizations
- Army Research Office
- National Institute of Allergy and Infectious Diseases
- National Institute of General Medical Sciences
- Pasteur Institute
- Texas Tech University
- Texas Tech University Health Sciences Center
- University of Texas at Austin