Dataset Information

Proteomics of Streptococcus mutans to Reveal the Antibiofilm Formation Mechanism of Ag/ZnO Nanocomposites with Light-Emitting Diode Radiation.

ABSTRACT:

Introduction

As a biofilm-associated disease, dental caries benefits from nanoparticle (NP)-based therapies. Streptococcus mutans (S. mutans) is a primary aetiologic agent for dental caries development. We successfully applied a synergistic therapy of Ag/ZnO nanocomposites combined with light-emitting diode (LED) radiation to inhibit S. mutans biofilms. However, the antibiofilm mechanism has not been fully elucidated, and little is known about the biofilm formation ability of bacteria that survive NP-based therapies.

Methods

This study explored the antibiofilm formation mechanism of this synergistic therapy by an integrated approach based upon proteomics.

Results

Synergistic therapy killed 99.8% of bacteria, while the biofilm formation ability of 0.2% surviving bacteria was inhibited. The proteomic responses of S. mutans to synergistic therapy were comprehensively characterized to unveil the mechanism of bacterial death and biofilm formation inhibition of the surviving bacteria. In total, 55 differentially expressed proteins (12 upregulated and 43 downregulated) were recorded. The bioinformatic analysis demonstrated that cellular integrity damage and regulated expression of structure-associated proteins were the main reasons for bacterial death. In addition, the proteomic study indicated the potential inhibition of metabolism in surviving bacteria and provided a biofilm-related network consisting of 17 differentially expressed proteins, explaining the multiantibiofilm formation actions. Finally, we reported and verified the inhibitory effects of synergistic therapy on sucrose metabolism and D-alanine metabolism, which disturbed the biofilm formation of surviving bacteria.

Conclusion

Our findings demonstrated that synergistic therapy killed most bacteria and inhibited the surviving bacteria from forming biofilms. Furthermore, the antibiofilm formation mechanism was revealed by proteomics analysis of S. mutans after synergistic therapy and subsequent metabolic studies. Our success may provide a showcase to explore the antibiofilm formation mechanism of NP-based therapies using proteomic studies.

SUBMITTER: Jiang N

PROVIDER: S-EPMC8612293 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundStreptococcus mutans (S. mutans) is one of the main cariogenic bacteria for caries. It was found that the clinical strains of S. mutans isolated from caries active population have stronger cariogenic ability than the isolates from caries-free (CF) people. Previous studies have found that curcumin can inhibit biofilm formation of S. mutans UA159. The objective of this study is to explore the antibiofilm effect of curcumin on the clinical isolates of S. mutans from severe early childhood caries(SECC).ResultsThe isolates from SECC group had more biomass than CF group (t = 4.296, P < 0.001). The acidogenicity and aciduricity of the strains from two groups showed no significant difference. After treatment with curcumin, the viability of biofilm was reduced to 61.865% ± 7.108% in SECC and to 84.059% ± 10.227% in CF group at 24 h (P < 0.05). The net reduction of live bacteria and total bacteria in the SECC group was significantly higher than that of the CF group (live bacteria t = 3.305, P = 0.016; total bacteria t = 2.378, P = 0.045) at 5 min. For 24 h, the net reduction of live bacteria and total bacteria in the SECC group was significantly higher than that of the CF group (live bacteria t = 3.305, P = 0.016; total bacteria t = 2.378, P = 0.045). The reduction of biofilm thickness reduced significantly in 5 min (t = 4.110, P = 0.015) and in 24 h (t = 3.453, P = 0.014). Long-term (24 h) curcumin treatment inhibited the amount of EPS in SECC group from (25.980 ± 1.156) μm3/μm2 to (20.136 ± 1.042) μm3/μm2, the difference was statistically significant (t = 7.510, P < 0.001). The gene of gtfC, gtfD, ftf, gbpB, fruA and srtA in the CF group and the gtfB, gtfC, gtfD, ftf, gbpB, srtA in SECC group were respectively reduced after 5 min curcumin treatment. After 24 h treatment, the gtfB, gtfC, gtfD, ftf, gbpB, fruA and srtA in both two groups were downregulation, all the differences were statistically significant.ConclusionsCurcumin has antibiofilm activity on clinical strains of S. mutans, especially for those isolated from SECC.