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胞外多糖基质:致龋生物膜的毒力决定因素。

The exopolysaccharide matrix: a virulence determinant of cariogenic biofilm.

机构信息

Center for Oral Biology, University of Rochester Medical Center, Rochester, NY, USA.

出版信息

J Dent Res. 2013 Dec;92(12):1065-73. doi: 10.1177/0022034513504218. Epub 2013 Sep 17.

Abstract

Many infectious diseases in humans are caused or exacerbated by biofilms. Dental caries is a prime example of a biofilm-dependent disease, resulting from interactions of microorganisms, host factors, and diet (sugars), which modulate the dynamic formation of biofilms on tooth surfaces. All biofilms have a microbial-derived extracellular matrix as an essential constituent. The exopolysaccharides formed through interactions between sucrose- (and starch-) and Streptococcus mutans-derived exoenzymes present in the pellicle and on microbial surfaces (including non-mutans) provide binding sites for cariogenic and other organisms. The polymers formed in situ enmesh the microorganisms while forming a matrix facilitating the assembly of three-dimensional (3D) multicellular structures that encompass a series of microenvironments and are firmly attached to teeth. The metabolic activity of microbes embedded in this exopolysaccharide-rich and diffusion-limiting matrix leads to acidification of the milieu and, eventually, acid-dissolution of enamel. Here, we discuss recent advances concerning spatio-temporal development of the exopolysaccharide matrix and its essential role in the pathogenesis of dental caries. We focus on how the matrix serves as a 3D scaffold for biofilm assembly while creating spatial heterogeneities and low-pH microenvironments/niches. Further understanding on how the matrix modulates microbial activity and virulence expression could lead to new approaches to control cariogenic biofilms.

摘要

许多人类传染病是由生物膜引起或加剧的。龋齿就是一个依赖生物膜的疾病的典型例子,它是由微生物、宿主因素和饮食(糖)相互作用引起的,这些因素调节了牙齿表面生物膜的动态形成。所有生物膜都有微生物衍生的细胞外基质作为必需成分。通过在菌膜和微生物表面(包括非变异链球菌)上存在的蔗糖(和淀粉)和变形链球菌衍生的外切酶之间的相互作用形成的胞外多糖,为致龋菌和其他生物提供了结合位点。原位形成的聚合物将微生物包裹起来,同时形成一个基质,促进三维(3D)多细胞结构的组装,这些结构包含一系列微环境,并牢固地附着在牙齿上。嵌入在富含胞外多糖和扩散受限基质中的微生物的代谢活性导致环境酸化,最终导致牙釉质的酸溶解。在这里,我们讨论了有关胞外多糖基质的时空发展及其在龋齿发病机制中的重要作用的最新进展。我们重点介绍了基质如何作为生物膜组装的 3D 支架,同时创造空间异质性和低 pH 微环境/小生境。进一步了解基质如何调节微生物活性和毒力表达,可能会导致控制致龋生物膜的新方法。

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