Probiotics have aroused increasing concern as an intervention strategy for periodontitis (PD), but their underlying mechanism of action remains poorly characterized. Regarding the significance of oral microbiota dysbiosis related to PD, we predicted that the preventive activity of probiotics may be influenced by suppressing the bacterial pathogenicity. Herein, we investigated the effects of Lactobacillus paracasei L9 (L9) and Bifidobacterium animalis A6 (A6) on PD using a rat model, and demonstrated a regulatory effect of probiotics on oral flora from a metagenomics perspective. Oral administration of A6 or L9 effectively relieved gingival bleeding, periodontal inflammatory infiltration, and alveolar bone resorption. In addition, A6 or L9 treatment reduced the inflammatory response and increased the expression of anti-inflammatory cytokines, which we expected to ameliorate alveolar bone resorption as mediated by the receptor activator of the nuclear factor-κB ligand/OPG signaling pathway. More importantly, using metagenomic sequencing, we showed that probiotics significantly altered the taxonomic composition of the subgingival microbiome, and reduced the relative proportions of pathogenic bacterial genera such as Streptococcus, Fusobacterium, Veillonella, and Escherichia. Both probiotics significantly inhibited levels of bacterial virulence factors related to adherence, invasion, exoenzyme, and complement protease functions that are strongly correlated with the pathogenesis of PD. Our overall results suggest that A6 and L9 may constitute promising prophylactic agents for PD, and should thus be further explored in the future.

Probiotics have been increasingly investigated for their role in alleviating symptoms of ulcerative colitis (UC), but the specific mechanism involved remains unclear. We investigated the alleviating effect of Bifidobacterium animalis A6 (BAA6) in UC through a mouse dextran sulfate sodium (DSS) model. When treated with a high dose of BAA6 (1 × 10 10 cfu/ml), it was found that colitis symptoms were significantly alleviated, and mucosal damages experienced obvious relief. Moreover, a high dose of BAA6 effectively upregulated free fatty acid receptors 2 and 3 (FFAR2 and FFAR3) expression and butyric acid metabolism specifically. Furthermore, the supplement of BAA6 significantly suppressed pro‐inflammatory cytokines levels (interleukin‐13) and the expression of pore‐forming protein claudin‐2. The upstream regulatory genes of claudin‐2, such as STAT6 , GATA4 , Cdx2 , were also significantly inhibited by BAA6. Collectively, this study concludes that BAA6 attenuated DSS‐induced colitis by increasing the levels of intestinal butyric acid, activating the butyric acid‐FFAR pathway, suppressing excessive proinflammatory response, and protecting the function of the colon epithelial barrier.

Oral microbial dysbiosis is the primary etiologic factor for halitosis, which may be the critical preventive target for halitosis. This study included randomized controlled trials (RCT) assessing the effects of...

Dental caries is a common and multifactorial biofilm disease that is associated with dietary habits and microbiota. Among the various pathogens inducing caries, S. mutans is the most extensively studied. Promoting oral health with probiotics has gained considerable attention. Lactobacillus paracasei (L. paracasei) strains were reported to modulate the gut microbiota and enhance host resistance to disease. Our previous research has found that L. paracasei ET-22 (ET-22) could inhibit S. mutans biofilms in vitro. However, the preventive effect in vivo and functional mechanism of ET-22 on dental caries were unclear. In this study, the preventive effects of ET-22 on dental caries in mice were checked. Meanwhile, the functional mechanism of ET-22 was further investigated. Results showed that the supplementation of ET-22 in drinking water significantly improved the caries scoring of mice. The microbiota of dental plaques revealed that the live and heat-killed ET-22 similarly regulated the microbial structure in plaque biofilms. Functional prediction of PICRUSt showed that the addition of live and heat-killed ET-22 may inhibit biofilm formation. By the in vitro trials, the live and heat-killed ET-22 indeed inhibited the construction of S. mutans biofilms and EPS productions of biofilms. This evidence suggests that ET-22 can restrain dental caries by regulating the microbiota of dental plaques and inhibiting biofilm formation, which may be partly mediated by the body components of ET-22.