Role of the luxS Quorum-Sensing System in Biofilm Formation and Virulence of Staphylococcus epidermidis

• Published in: Infection and Immunity Vol. 74; no. 1; pp. 488 - 496
• Main Authors: Xu, Lin, Li, Hualin, Vuong, Cuong, Vadyvaloo, Viveka, Wang, Jianping, Yao, Yufeng, Otto, Michael, Gao, Qian
• Format: Journal Article
• Language: English
• Published: Washington, DC American Society for Microbiology 2006
• Subjects: Animals; Bacterial Proteins - genetics; Bacterial Proteins - physiology; Bacteriology; Biofilms - growth & development; Biological and medical sciences; Carbon-Sulfur Lyases; Cross Infection - metabolism; Disease Models, Animal; Fundamental and applied biological sciences. Psychology; Homoserine - analogs & derivatives; Homoserine - metabolism; Humans; Lactones - metabolism; Male; Microbiology; Microscopy, Electron, Scanning; Miscellaneous; Molecular Pathogenesis; Mutation; Rats; Rats, Sprague-Dawley; Staphylococcal Infections - metabolism; Staphylococcal Infections - microbiology; Staphylococcus epidermidis; Staphylococcus epidermidis - genetics; Staphylococcus epidermidis - pathogenicity; Staphylococcus epidermidis - physiology; Staphylococcus epidermidis - ultrastructure; Virulence; Staphylococcus epidermidis; Microbiology; Virulence; Biofilm; Bacteria; Micrococcales; Micrococcaceae; Quorum sensing; Immunity
• ISSN: 0019-9567; 1098-5522
• DOI: 10.1128/IAI.74.1.488-496.2006

Nosocomial infections caused by Staphylococcus epidermidis are characterized by biofilm formation on implanted medical devices. Quorum-sensing regulation plays a major role in the biofilm development of many bacterial pathogens. Here, we describe luxS, a quorum-sensing system in staphylococci that has a significant impact on biofilm development and virulence. We constructed an isogenic [Delta]luxS mutant strain of a biofilm-forming clinical isolate of S. epidermidis and demonstrated that luxS signaling is functional in S. epidermidis. The mutant strain showed increased biofilm formation in vitro and enhanced virulence in a rat model of biofilm-associated infection. Genetic complementation and addition of autoinducer 2-containing culture filtrate restored the wild-type phenotype, demonstrating that luxS repressed biofilm formation through a cell-cell signaling mechanism based on autoinducer 2 secretion. Enhanced production of the biofilm exopolysaccharide polysaccharide intercellular adhesin in the mutant strain is presumably the major cause of the observed phenotype. The agr quorum-sensing system has previously been shown to impact biofilm development and biofilm-associated infection in a way similar to that of luxS, although by regulation of different factors. Our study indicates a general scheme of quorum-sensing regulation of biofilm development in staphylococci, which contrasts with that observed in many other bacterial pathogens.