Chi Yaqi, Wang Ye, Fu Di, Yao Lin, Wei Mingying, Zhou Ge, Yang Guang, Zou Ling, Ren Biao
State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Department of Endodontics, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
J Oral Microbiol. 2025 Feb 12;17(1):2465345. doi: 10.1080/20002297.2025.2465345. eCollection 2025.
Caries is one of the most common diseases worldwide, and is considered to be the primary cariogenic pathogen of dental caries. Sodium houttuyfonate (SH) has showed potential antibacterial effects, however, its actions and mechanisms on and cariogenicity remain unclear and need further study.
we investigated the effects of SH on the cariogenic ability of , including growth, biofilm formation, exopolysaccharides (EPS) and acid productions. RNA-Seq and mutants' validation were also performed to explore the mechanisms of SH on . The dental caries rat model was finally employed to evaluate the anti-caries capabilities of SH.
The MIC of SH against was 64 μg/mL. SH inhibited biofilm formation and cariogenic virulence of , including EPS and acid productions, in a dose-dependent manner. RNA-seq analysis indicated that SH significantly downregulated the VicRK pathway, a key pathway regulating biofilm formation and EPS generation. The , , and mutants were more sensitive to SH, while and overexpression strains and were more resistant to SH than WT strains, indicating that SH downregulated the pathway to inhibit the cariogenicity of . SH also significantly inhibited the development of dental caries in rats without systematic toxicities. The expressions of , , and genes from rat plaques were downregulated by SH.
This study suggested SH inhibited the cariogenic virulence of through the downregulation of VicRK two components pathway, thereby offering novel insights for clinical caries prevention.
龋齿是全球最常见的疾病之一，被认为是龋齿的主要致龋病原体。鱼腥草素钠（SH）已显示出潜在的抗菌作用，然而，其对变形链球菌及其致龋性的作用和机制仍不清楚，需要进一步研究。
我们研究了SH对变形链球菌致龋能力的影响，包括生长、生物膜形成、胞外多糖（EPS）和酸产生。还进行了RNA测序和突变体验证，以探索SH对变形链球菌的作用机制。最终采用龋齿大鼠模型评估SH的防龋能力。
SH对变形链球菌的最低抑菌浓度为64μg/mL。SH以剂量依赖性方式抑制变形链球菌的生物膜形成和致龋毒力，包括EPS和酸产生。RNA测序分析表明，SH显著下调了VicRK途径，这是调节生物膜形成和EPS产生的关键途径。comC、comD、comE和covR突变体对SH更敏感，而comC和covR过表达菌株SA-COM-C和SA-COM-R比野生型菌株对SH更具抗性，表明SH下调comC途径以抑制变形链球菌的致龋性。SH还显著抑制大鼠龋齿的发展，且无全身毒性。SH下调了大鼠菌斑中comC、comD、comE和covR基因的表达。
本研究表明，SH通过下调VicRK双组分途径抑制变形链球菌的致龋毒力，从而为临床龋齿预防提供了新的见解。
