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 and being the two most commonly isolated species. While readily kills, 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 and We demonstrate that 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 to produce virulence factors that kill These data could provide important clues regarding the virulence of in albumin-depleted versus albumin-rich infection sites and an understanding of the nature of friendly versus antagonistic interactions between and.

RhlR-Regulated Acyl-Homoserine Lactone Quorum Sensing in a Cystic Fibrosis Isolate of Pseudomonas aeruginosa

“…Thereafter, 3D cell cultures were equally distributed in a 48-well plate at a concentration of 2.5 ϫ 10 5 cells/well (250-l volume), and infected with the different strains at a targeted multiplicity of infection of 30:1 as described previously (44). All infection studies were performed in the above-described cell culture medium, with the exception that no FBS was added given the interference of serum compounds with QS signaling (58). After 24 h of infection, the release of cytosolic lactate dehydrogenase (LDH) from 3D lung epithelial cell cultures was determined using an LDH activity assay kit (Sigma-Aldrich) according to the manufacturer's instructions.…”

Non-hierarchical, RhlR-regulated acyl-homoserine lactone quorum sensing in a cystic fibrosis isolate ofPseudomonas aeruginosa

“…Thereafter, 3-D cell cultures were equally distributed in a 48-well plate at a concentration of 2.5 × 10 5 cells/well (250 μL volume), and infected with the different strains at a targeted multiplicity of infection of 30:1 as described previously[43]. All infection studies were performed in the above-described cell culture medium, with the exception that no FBS was added given the interference of serum compounds with QS signaling [57]. After 24 h infection, the release of cytosolic lactate dehydrogenase (LDH) from 3-D lung epithelial cell cultures was determined using a LDH activity assay kit (Sigma-Aldrich) according to the manufacturer’s instructions.…”

Social behaviours by Bacillus subtilis: quorum sensing, kin discrimination and beyond

“…This is not specific to Bacillus species as similar findings have also been shown for Pseudomonas aeruginosa and Staphylococcus aureus which usually do not coexist, as P. aeruginosa outcompetes S. aureus through production of molecules that are under the control of QS systems. In the blood however, QS signalling is inhibited in P. aeruginosa due to binding on serum albumin to QS molecules, resulting in coexistence of the two organisms (Smith et al, ). Therefore, it will be interesting to address the relationship between kin discrimination, quorum sensing and cheating in the formation, competitive fitness and spatial organisation of cells within in environmental biofilms and couple this with an analysis of the impact exerted by diverse environmental settings.…”