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Quorum sensing (QS) has been recognized to play an important role in many pathogenic bacteria, and has become a novel target for the treatment of infectious disease.Pseudomonas aeruginosa is highly resistant to antibiotic treatment, largely due to its ability to form biofilms, and QS was found to be essential for the creation of mature, differentiated biofilms in this organism.A novel QS inhibitor, C2 (N-DecanoyI-L-homoserine benzyl ester), can attenuate not only total protease and elastase activity, but also swarming motility and biofilm formation in the Pseudomonas aeruginosa strain PAO1.We demonstrated that C2 showed a significant inhibitory effect on biofilm formation in a dose-dependent manner.In the presence of 200 μM C2,PAO1 biofilm formation dropped to 36.92% in normal saline, 21.87% in LB liquid medium, and 18.03% in LB liquid medium containing 50 μg/ml tobramycin.Data from cDNA microarray showed that expression of 382 genes (~6.4%) was significantly different (P value<0.05) with C2 treatment, including down-regulation of 215 genes (~3.6%) and up-regulation of 167 genes (~2.8%).Real-time RT-PCR showed that the gene qscR, which encodes the LuxR-type receptor QscR (quorum sensing control repressor), was significantly up-regulated by 375.4% during C2treatment.The mechanism by which C2 inhibits biofilm formation may be through repression of Las and Rhl systems by QscR.C2 was shown to reduce biofilm formation and block the antibiotic tolerance of biofilms.Further, in combination with antibiotics, it abolishes biofilm formation completely.This result may pave the way for new treatments for biofilm-related infections, and may be exploited for the general prevention of biofilm formation.