Division of Microbiology and Infectious Diseases, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Department of Microbiology and Infection Control Sciences, Kyoto Pharmaceutical University, Kyoto, Japan.
Microbiol Immunol. 2020 Jul;64(7):493-501. doi: 10.1111/1348-0421.12797. Epub 2020 Jun 8.
Streptococcus mutans is the main pathogen of dental caries and adheres to the tooth surface via soluble and insoluble glucans produced by the bacterial glucosyltransferase enzyme. Thus, the S. mutans glucosyltransferase is an important virulence factor for this cariogenic bacterium. Sulfated vizantin effectively inhibits biofilm formation by S. mutans without affecting its growth. In this study, less S. mutans biofilm formation occurred on hydroxyapatite discs coated with sulfated vizantin than on noncoated discs. Sulfated vizantin showed no cytotoxicity against the human gingival cell line Ca9-22. Sulfated vizantin dose-dependently inhibited the extracellular release of cell-free glucosyltransferase from S. mutans and enhanced the accumulation of cell-associated glucosyltransferase, compared with that observed with untreated bacteria. Sulfated vizantin disrupted the localization balance between cell-associated glucosyltransferase and cell-free glucosyltransferase, resulting in inhibited biofilm maturation. These results indicate that sulfated vizantin can potentially serve as a novel agent for preventing dental caries.
变形链球菌是龋齿的主要病原体,通过细菌葡糖基转移酶产生的可溶性和不溶性葡聚糖黏附在牙齿表面。因此,变形链球菌葡糖基转移酶是这种致龋细菌的重要毒力因子。硫酸 vizantin 可有效抑制变形链球菌生物膜的形成,而不影响其生长。在本研究中,涂有硫酸 vizantin 的羟基磷灰石片上形成的变形链球菌生物膜比未涂覆的片上少。硫酸 vizantin 对人牙龈细胞系 Ca9-22 无细胞毒性。与未经处理的细菌相比,硫酸 vizantin 呈剂量依赖性地抑制游离葡糖基转移酶从变形链球菌中的细胞外释放,并增加细胞相关葡糖基转移酶的积累。硫酸 vizantin 破坏了细胞相关葡糖基转移酶和游离葡糖基转移酶之间的定位平衡,从而抑制了生物膜的成熟。这些结果表明,硫酸 vizantin 可能是一种预防龋齿的新型药物。