Abstract
Biofilms significantly enhance antibiotic resistance by inhibiting penetration of antibiotics and are shielded from the immune system via the formation of an extracellular polymeric matrix. Innovative and novel approaches are required for the inhibition of biofilm formation and treatment of biofilm-associated infectious diseases. In the current study, a biofilm model of Staphylococcus aureus was established in vitro to explore inhibitory effects of brazilin (BN) on biofilm formation and to evaluate damaging effects of BN in the presence and absence of vancomycin (VCM) on the biofilm. Antibiofilm-infection mechanisms of BN were observed. In these experiments, the clinical strain of S. aureus C-4-4 was isolated for biofilm formation. Crystal violet staining and fluorescence microscopy revealed that BN inhibited biofilm formation in vitro and the best effect was observed with two times the minimum inhibitory concentration of BN following 48 h incubation. Additionally, the results demonstrated that BN in combination with VCM enhanced the damage to biofilms, whereas VCM alone did not. The results of the reverse transcription-quantitative polymerase chain reaction analyses demonstrated that BN downregulated gene expression of intercellular adhesion (ica)A and upregulated icaR and the quorum-sensing (QS) system regulator accessory gene regulator A. In summary, BN inhibited S. aureus biofilm formation and destroyed biofilms, while simultaneously increasing permeability to VCM. BN was able to reduce production of the extracellular polymeric matrix and inhibited the QS system. These results support the use of BN as a novel drug and treatment strategy for S. aureus biofilm-associated infections.