Role of the SaeRS two-component regulatory system in Staphylococcus epidermidisautolysis and biofilm formation

Qiang Lou,Tao Zhu,Adrien Fischer,Yang Wu,Di Qu,Jingran Liu,Patrice Francois,Jian Hu,Haijing Ben,Jacques Schrenzel,Fangyou Yu,Jinsong Yang

doi:10.1186/1471-2180-11-146

Abstract

BackgroundStaphylococcus epidermidis (SE) has emerged as one of the most important causes of nosocomial infections. The SaeRS two-component signal transduction system (TCS) influences virulence and biofilm formation in Staphylococcus aureus. The deletion of saeR in S. epidermidis results in impaired anaerobic growth and decreased nitrate utilization. However, the regulatory function of SaeRS on biofilm formation and autolysis in S. epidermidis remains unclear.ResultsThe saeRS genes of SE1457 were deleted by homologous recombination. The saeRS deletion mutant, SE1457ΔsaeRS, exhibited increased biofilm formation that was disturbed more severely (a 4-fold reduction) by DNase I treatment compared to SE1457 and the complementation strain SE1457saec. Compared to SE1457 and SE1457saec, SE1457ΔsaeRS showed increased Triton X-100-induced autolysis (approximately 3-fold) and decreased cell viability in planktonic/biofilm states; further, SE1457ΔsaeRS also released more extracellular DNA (eDNA) in the biofilms. Correlated with the increased autolysis phenotype, the transcription of autolysis-related genes, such as atlE and aae, was increased in SE1457ΔsaeRS. Whereas the expression of accumulation-associated protein was up-regulated by 1.8-fold in 1457ΔsaeRS, the expression of an N-acetylglucosaminyl transferase enzyme (encoded by icaA) critical for polysaccharide intercellular adhesin (PIA) synthesis was not affected by the deletion of saeRS.ConclusionsDeletion of saeRS in S. epidermidis resulted in an increase in biofilm-forming ability, which was associated with increased eDNA release and up-regulated Aap expression. The increased eDNA release from SE1457ΔsaeRS was associated with increased bacterial autolysis and decreased bacterial cell viability in the planktonic/biofilm states.

Highlights

Staphylococcus epidermidis (SE) has emerged as one of the most important causes of nosocomial infections
Effect of saeRS deletion on S. epidermidis biofilm formation In order to explore the influence of saeR and saeS on S. epidermidis biofilm formation, an S. epidermidis 1457ΔsaeRS mutant (SE1457ΔsaeRS) and a complemented strain (SE1457saec) were constructed using the shuttle plasmids pMAD and pBT2, respectively
It did not reach the level of the wild-type strain, complementation of saeRS resulted in decreased biofilm formation (Student’s t-test, P < 0.05) (Figure 1)

Summary

Introduction

Staphylococcus epidermidis (SE) has emerged as one of the most important causes of nosocomial infections. The SaeRS two-component signal transduction system (TCS) influences virulence and biofilm formation in Staphylococcus aureus. The opportunistic pathogen Staphylococcus epidermidis has emerged as an important etiologic agent of nosocomial infections. The ability to form biofilms on the surfaces of medical devices is an important component of S. epidermidis pathogenicity. During the bacterial accumulation phase in S. epidermidis, biofilm formation is mediated by extracellular polysaccharides and proteins, such as polysaccharide intercellular adhesin (PIA) [3] and accumulation-associated protein (Aap) [4]. Extracellular DNA release from S. epidermidis is related to AtlE-mediated bacterial autolysis [7]. Another autolysin recently identified in S. epidermidis, Aae, has bacteriolytic activities and adhesive properties [8]

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