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Abstract
Quorum sensing (QS) is a means of cell-to-cell communication that uses diffusible signaling molecules that are sensed by the population to determine population density, thus allowing co-ordinate gene regulation in response to population density. In Pseudomonas aeruginosa, production of the QS signaling molecule, N-acyl homoserine lactone (AHL), co-ordinates expression of key factors of pathogenesis, including biofilm formation and toxin secretion. It is predicted that the inhibition of AHL sensing would provide an effective clinical treatment to reduce the expression of virulence factors and increase the effectiveness of antimicrobial agents. We previously demonstrated that sodium houttuyfonate (SH), commonly used in traditional Chinese medicine to treat infectious diseases, can effectively inhibit QS-regulated processes, including biofilm formation. Here, using a model system, we demonstrate that SH causes the dose-dependent inhibition of AHL production, through down-regulation of the AHL biosynthesis gene, lasI. Addition of SH also resulted in down-regulation of expression of the AHL sensor and transcriptional regulator, LasR, and inhibited the production of the QS-regulated virulence factors, pyocyanin and LasA. These results suggest that the antimicrobial activity of SH may be due to its ability to disrupt QS in P. aeruginosa.
Highlights
The Gram-negative opportunistic pathogen, Pseudomonas aeruginosa, is a typical biofilm-forming microbe, and this characteristic allows it to thrive in a diverse range of natural and nosocomial niches (Driscoll et al, 2007)
We found the minimum inhibitory concentrations (MICs) for P. aeruginosa strain ATCC27853 to be 512 μg/ml and 64 μg/ml, respectively
The quorum sensing system is a key regulatory system which is responsible for the multi-drug resistance and pathogenesis of P. aeruginosa (Van Delden and Iglewski, 1998)
Summary
The Gram-negative opportunistic pathogen, Pseudomonas aeruginosa, is a typical biofilm-forming microbe, and this characteristic allows it to thrive in a diverse range of natural and nosocomial niches (Driscoll et al, 2007). Co-ordination of gene expression through QS is an important determinant of virulence and drug-resistance in P. aeruginosa (Van Delden and Iglewski, 1998). P. aeruginosa utilizes two interconnected QS systems, termed Las and Rhl (Schuster et al, 2013), which are regulated by N-acyl-homoserine lactones (AHLs, termed P. aeruginosa autoinducers; PAIs). LasI synthesizes the AHL molecule, N-3-oxododecanoyl-L-homoserine lactone (3OC12-HSL, PAI-1), which is bound by the transcription regulator, LasR (Pearson et al, 1994). LasR directly regulates the expression of up to 74 genes, including lasI (Gilbert et al, 2009). In the analogous Rhl system, RhlI synthesizes N-butyrylL-homoserine lactone (C4-HSL, PAI-2) and RhlR acts as the sensor/transcriptional regulator (Brint and Ohman, 1995)
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