Exploration of the primary antibiofilm substance and mechanism employed by ATCC 11741 to inhibit biofilm of .

INTRODUCTION

serves as a probiotic potentially capable of preventing dental caries both and . This study focused on understanding the key antibiofilm agents and the mechanisms of action of the supernatant against .

METHODS

biofilm was constructed and the cell-free supernatant of was added. After the biofilm was collected, RNA-seq and qRT-PCR were then performed to get gene information. The influence of temperature, pH and other factors on the supernatant were measured and non-targeted metabolome analysis was performed to analyze the effective components.

RESULTS

The findings indicated that the supernatant derived from could inhibit the biofilm formation of mutans at different times. Through transcriptome analysis, we discovered that the cell-free supernatant reduced biofilm formation, by suppressing phosphoenolpyruvate-dependent phosphotransferase systems along with two ATP-binding cassette transporters, rather than directly affecting the genes that code for glucosyltransferases; additionally, the supernatant was observed to diminish the expression of genes linked to two-component systems, polyketides/non-ribosomal peptides, acid stress response, quorum sensing, and exopolysaccharide formation. Non-targeted LC-MS/MS analysis was employed to discover a variety of potential active compounds present in the cellular filtrate of that hinder the growth of S. mutans, including phenyllactic acid, sorbitol, and honokiol.

DISCUSSION

In summary, our findings support the evaluation of as a promising oral probiotic aimed at hindering the formation of biofilms by cariogenic pathogens and the development of dental caries.