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Background   Staphylococcus aureus  is an important pathogen that causes biofilm-associated infection in humans. Autoinducer 2 (AI-2), a quorum-sensing (QS) signal for interspecies communication, has a wide range of regulatory functions in both Gram-positive and Gram-negative bacteria, but its exact role in biofilm formation in  S. aureus  remains unclear.    Results  Here we demonstrate that mutation of the AI-2 synthase gene  luxS  in  S. aureus  RN6390B results in increased biofilm formation compared with the wild-type (WT) strain under static, flowing and anaerobic conditions and in a mouse model. Addition of the chemically synthesized AI-2 precursor in the  luxS  mutation strain (ΔluxS) restored the WT phenotype. Real-time RT-PCR analysis showed that AI-2 activated the transcription of  icaR , a repressor of the  ica  operon, and subsequently a decreased level of  icaA  transcription, which was presumably the main reason why  luxS  mutation influences biofilm formation. Furthermore, we compared the roles of the  agr -mediated QS system and the LuxS/AI-2 QS system in the regulation of biofilm formation using the ΔluxS strain, RN6911 and the Δagr ΔluxS strain. Our data indicate a cumulative effect of the two QS systems on the regulation of biofilm formation in  S. aureus .    Conclusion  These findings demonstrate that AI-2 can decrease biofilm formation in  S. aureus  via an  icaR -activation pathway. This study may provide clues for therapy in  S. aureus  biofilm-associated infection.

Staphylococcus aureus autoinducer-2 quorum sensing decreases biofilm formation in an icaR-dependent manner