Autoinducer-2 regulates Pseudomonas aeruginosa PAO1 biofilm formation and virulence production in a dose-dependent manner.

Hongdong Li,Jialin Yu,Yakun Fu,Xingyuan Li,Ying Dong,Zhengli Wang,Qing Ai

doi:10.1186/s12866-015-0529-y

Abstract

BackgroundPseudomonas aeruginosa is an opportunistic pathogen that is the leading cause of iatrogenic infections in critically ill patients, especially those undergoing mechanical ventilation. In this study, we investigated the effects of the universal signaling molecule autoinducer-2 (AI-2) in biofilm formation of P. aeruginosa PAO1.ResultsThe addition of 0.1 nM, 1 nM, and 10 nM exogenous AI-2 to P. aeruginosa PAO1 increased biofilm formation, bacterial viability, and the production of virulence factors. However, compared to the 10 nM AI-2 group, higher concentrations of AI-2 (100 nM and 1 μM) reduced biofilm formation, bacterial viability, and the production of virulence factors. Consistent with the changes in morphology, gene expression analysis revealed that AI-2 up-regulated the expression of quorum sensing-associated genes and genes encoding virulence factors at lower concentrations and down-regulated these genes at higher concentrations.ConclusionsOur study demonstrated that exogenous AI-2 acted in a dose-dependent manner to regulate P. aeruginosa biofilm formation and virulence factors secretion via modulating the expression of quorum sensing-associated genes and may be targeted to treat P. aeruginosa biofilm infections.

Highlights

Pseudomonas aeruginosa is an opportunistic pathogen that is the leading cause of iatrogenic infections in critically ill patients, especially those undergoing mechanical ventilation
Effects of AI-2 on P. aeruginosa growth To test the impact of AI-2 on P. aeruginosa biofilm formation and virulence, we first investigated its effect on planktonic bacterial growth
Biofilm formation increased in the presence of 0.1 nM, 1 nM, and 10 nM AI-2 with a 1.1, 1.3, and 1.4-fold increase in biofilm biomass compared to the negative control

Summary

Introduction

Pseudomonas aeruginosa is an opportunistic pathogen that is the leading cause of iatrogenic infections in critically ill patients, especially those undergoing mechanical ventilation. We investigated the effects of the universal signaling molecule autoinducer-2 (AI-2) in biofilm formation of P. aeruginosa PAO1. P. aeruginosa could produce a number of virulence factors, such as pyocyanin, rhamnolipids, elastase, exotoxin A, phospholipase C, and exoenzyme S, which are thought to be involved in acute or chronic infections [3]. Autoinducer-2 (AI-2) is a universal QS molecule that mediates intra- and interspecies communication. This molecule is formed from spontaneous rearrangement of 4, 5-dihydroxy-2, 3-pentanedione (DPD), which is produced by the enzyme LuxS, and is the primary QS molecule produced by many Gram-positive and Gram-negative bacteria. An example is reported in the study conducted by Geier et al, where AI-2 increased biofilm formation by Mycobacterium avium, which cannot produce AI-2 [14]

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Conclusion