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通过靶向胞外多糖代谢的策略抑制生物膜形成。

Inhibition of biofilm formation by strategies targeting the metabolism of exopolysaccharides.

机构信息

State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.

出版信息

Crit Rev Microbiol. 2021 Sep;47(5):667-677. doi: 10.1080/1040841X.2021.1915959. Epub 2021 May 3.

DOI:10.1080/1040841X.2021.1915959
PMID:33938347
Abstract

Dental caries is one of the most prevalent and costly biofilm-associated infectious diseases affecting most of the world's population. In particular, dental caries is driven by dysbiosis of the dental biofilm adherent to the enamel surface. Specific types of acid-producing bacteria, especially , colonize the dental surface and cause damage to the hard tooth structure in the presence of fermentable carbohydrates. has been established as the major cariogenic pathogen responsible for human dental caries, with a high ability to form biofilms. The exopolysaccharide (EPS) matrix, mainly contributed by , has been considered as a virulence determinant of cariogenic biofilm. As EPS is an important virulence factor, targeting EPS metabolism could be useful in preventing cariogenic biofilm formation. This review summarizes plausible strategies targeting biofilms by degrading EPS structure, inhibiting EPS production, and disturbing the EPS metabolism-related gene expression and regulatory systems.

摘要

龋齿是一种最普遍且代价高昂的生物膜相关传染性疾病,影响着世界上大多数人口。特别是,龋齿是由黏附在牙釉质表面的牙生物膜失调引起的。特定类型的产酸细菌,特别是 ,定植在牙表面,并在可发酵碳水化合物存在的情况下对坚硬的牙齿结构造成损害。 已被确定为主要的致龋病原体,其具有形成生物膜的高能力。胞外多糖 (EPS) 基质主要由 贡献,被认为是致龋生物膜的毒力决定因素。由于 EPS 是一种重要的毒力因子,因此靶向 EPS 代谢可能有助于预防致龋生物膜的形成。这篇综述总结了通过降解 EPS 结构、抑制 EPS 产生以及干扰 EPS 代谢相关基因表达和调控系统来靶向 生物膜的合理策略。

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