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Background  The targeting of  Staphylococcus aureus  biofilm structures are now gaining interest as an alternative strategy for developing new types of antimicrobial agents. Magnolol (MOL) shows inhibitory activity against  S. aureus  biofilms and Triton X-100-induced autolysis  in vitro , although there are no data regarding the molecular mechanisms of MOL action in bacteria.    Methodology/Principal Findings  The molecular basis of the markedly reduced autolytic phenotype and biofilm inhibition triggered by MOL were explored using transcriptomic analysis, and the transcription of important genes were verified by real-time RT-PCR. The inhibition of autolysis by MOL was evaluated using quantitative bacteriolytic assays and zymographic analysis, and antibiofilm activity assays and confocal laser scanning microscopy were used to elucidate the inhibition of biofilm formation caused by MOL in 20 clinical isolates or standard strains. The reduction in  cidA ,  atl ,  sle1 , and  lytN  transcript levels following MOL treatment was consistent with the induced expression of their autolytic repressors  lrgA ,  lrgB ,  arlR , and  sarA . MOL generally inhibited or reversed the expression of most of the genes involved in biofilm production. The growth of  S. aureus  strain ATCC 25923 in the presence of MOL dose-dependently led to decreases in Triton X-100-induced autolysis, extracellular murein hydrolase activity, and the amount of extracellular DNA (eDNA). MOL may impede biofilm formation by reducing the expression of  cidA , a murein hydrolase regulator, to inhibit autolysis and eDNA release, or MOL may directly repress biofilm formation.    Conclusions/Significance  MOL shows  in vitro  antimicrobial activity against clinical and standard  S. aureus  strains grown in planktonic and biofilm cultures, suggesting that the structure of MOL may potentially be used as a basis for the development of drugs targeting biofilms.

Transcriptional and Functional Analysis of the Effects of Magnolol: Inhibition of Autolysis and Biofilms in Staphylococcus aureus