From Biofilm to\nBreath: The Role of <i>Lacticaseibacillus\nparacasei</i> ET-22 Postbiotics in Combating Oral Malodor

Previous studies demonstrated that sufferers with halitosis\ncan\nbe significantly improved with <i>Lacticaseibacillus paracasei</i> ET-22 (ET-22) postbiotics intervention. The objectives of this investigation\nwere to identify the primary components responsible for inhibiting\noral malodor. This study demonstrated that cell-free supernatants\n(CFSs) were more effective in inhibiting production of volatile sulfur\ncompounds (VSCs). Untargeted metabolomics identified CFSs as primarily\nconsisting of organic acids, lipids, peptides, and nucleotides. Among\nthe potential active components, phenyllactic acid (PLA) and peptide\nGP(Hyp)GAG significantly inhibited microbial-induced VSCs production,\nwith VSC concentrations reduced by 42.7% and 44.6%, respectively.\nGiven the correlation between biofilms and halitosis, microstructural\nchanges in biofilms were examined. PLA suppressed the biomass of the\nbiofilm by 41.7%, while the biofilm thickness was reduced from 202.3\nto 70.0 μm. GP(Hyp)GAG intervention reduced the abundance of <i>Fusobacterium nucleatum</i> and <i>Streptococcus mutans</i> within the biofilm, and the expression of biofilm-forming genes <i>FadA</i> and <i>Gtfb</i> were also suppressed by 41.8%\nand 59.4%. Additionally, the VSC production capacities were reduced\ndue to the decrease in VSC producing bacteria (<i>F. nucleatum</i>, <i>Prevotella intermedia</i>, and <i>Solobacterium\nmoorei</i>) and down-regulation of <i>Cdl</i> and <i>Mgl</i> genes. Collectively, the current study proved that PLA\nand GP(Hyp)GAG may be the main contributors to halitosis inhibition\nby ET-22 postbiotics.