The Tea Catechin Epigallocatechin Gallate Suppresses Cariogenic Virulence Factors of Streptococcus mutans

The Tea Catechin Epigallocatechin Gallate Suppresses Cariogenic Virulence Factors of Streptococcus mutans
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DOI:
10.1128/aac.01016-10
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发表时间:
2011-03-01
影响因子:
4.9
通讯作者:
Wu, Christine D.
Wu, Christine D.
中科院分区:
医学2区
文献类型:
--
作者:
Xu, Xin;Zhou, Xue D.;Wu, Christine D.

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变形链球菌是引起龋齿的主要病原体,具有一系列与致龋性相关的毒力因子。替代传统的抗菌治疗,药物选择性地抑制毒力因子,而不一定抑制常驻口腔物种,是有希望的。茶的抗肿瘤特性已在实验动物和人类中得到证实。茶多酚,特别是表没食子儿茶素没食子酸酯(EGCg),已经被证明可以抑制变形链球菌的生长和葡萄糖转移酶的活性。然而,除糖基转移酶外,它们对口腔链球菌生物膜和致龋毒力因子的影响尚未有很好的文献记载。在本研究中,我们研究了EGCg对变形链球菌毒力因子及其致酸性和酸度的生物学效应。研究了EGCg对化学培养基中生长的变形链球菌生物膜的抑菌作用。EGCg抑制变形链球菌浮游细胞生长的MIC为31.25 μ g/ml,最低杀菌浓度(MBC)为62.5 μ g/ml。EGCg在15.6 μ g/ml(最低抑制90%以上生物膜形成的浓度)时也能抑制变形链球菌生物膜的形成,在625 μ g/ml(无梗MIC80)时也能降低预成型生物膜的活力。亚mic水平的EGCg抑制变形链球菌细胞的致酸性和酸性。实时PCR数据分析显示,EGCg显著抑制变形链球菌UA159的ldh、eno、atpD和aguD基因。f1fo - atp酶和乳酸脱氢酶的酶活性也被抑制(50%的抑制浓度在15.6 ~ 31.25 μ g/ml之间)。这些发现表明EGCg是一种天然的抗致癌剂,因为它对变形链球菌具有抗菌活性,并抑制与其致癌性相关的特定毒力因子。
Streptococcus mutans, the primary etiologic agent of dental caries, possesses a series of virulence factors associated with its cariogenicity. Alternatives to traditional antimicrobial treatment, agents selectively inhibiting the virulence factors without necessarily suppressing the resident oral species, are promising. The anticariogenic properties of tea have been suggested in experimental animals and humans. Tea polyphenols, especially epigallocatechin gallate (EGCg), have been shown to inhibit the growth and glucosyltransferases activity of S. mutans. However, their effects on biofilm and cariogenic virulence factors of oral streptococci other than glucosyltransferases have not been well documented. In this study, we investigated the biological effect of EGCg on the virulence factors of S. mutans associated with its acidogenicity and acidurity. The antimicrobial effects of EGCg on S. mutans biofilm grown in chemically defined medium were also examined. EGCg inhibited growth of S. mutans planktonic cells at an MIC of 31.25 mu g/ml and a minimal bactericidal concentration (MBC) of 62.5 mu g/ml. EGCg also inhibited S. mutans biofilm formation at 15.6 mu g/ml (minimum concentration that showed at least 90% inhibition of biofilm formation) and reduced viability of the preformed biofilm at 625 mu g/ml (sessile MIC80). EGCg at sub-MIC levels inhibited acidogenicity and acidurity of S. mutans cells. Analysis of the data obtained from real-time PCR showed that EGCg significantly suppressed the ldh, eno, atpD, and aguD genes of S. mutans UA159. Inhibition of the enzymatic activity of F1Fo-ATPase and lactate dehydrogenase was also noted (50% inhibitory concentration between 15.6 and 31.25 mu g/ml). These findings suggest that EGCg is a natural anticariogenic agent in that it exhibits antimicrobial activity against S. mutans and suppresses the specific virulence factors associated with its cariogenicity.