| Summary: | <p>Abstract</p> <p>Background</p> <p><it>Staphylococcus aureus</it> 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 <it>S. aureus</it> remains unclear.</p> <p>Results</p> <p>Here we demonstrate that mutation of the AI-2 synthase gene <it>luxS</it> in <it>S. aureus</it> 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 <it>luxS</it> mutation strain (ΔluxS) restored the WT phenotype. Real-time RT-PCR analysis showed that AI-2 activated the transcription of <it>icaR</it>, a repressor of the <it>ica</it> operon, and subsequently a decreased level of <it>icaA</it> transcription, which was presumably the main reason why <it>luxS</it> mutation influences biofilm formation. Furthermore, we compared the roles of the <it>agr</it>-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 <it>S. aureus</it>.</p> <p>Conclusion</p> <p>These findings demonstrate that AI-2 can decrease biofilm formation in <it>S. aureus</it> via an <it>icaR</it>-activation pathway. This study may provide clues for therapy in <it>S. aureus</it> biofilm-associated infection.</p>
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