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Glucans synthesized in situ in experimental salivary pellicle function as specific binding sites for Streptococcus mutans.

机译:在实验唾液薄膜中原位合成的葡聚糖起变形链球菌的特异性结合位点的作用。

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Many researchers have suggested that the role of glucan-mediated interactions in the adherence of Streptococcus mutans is restricted to accumulation of this cariogenic bacterium following its sucrose (i.e., glucan)-independent binding to saliva-coated tooth surfaces. However, the presence of enzymatically active glucosyltransferase in salivary pellicle suggests that glucans could also promote the initial adherence of S. mutans to the teeth. In the present study, the commonly used hydroxyapatite adherence assay was modified to include the incorporation of glucosyltransferase and the synthesis of glucans in situ on saliva-coated hydroxyapatite beads. Several laboratory strains and clinical isolates of S. mutans were examined for their ability to adhere to experimental pellicles, either with or without the prior formation of glucans in situ. Results showed that most strains of S. mutans bound stereospecifically to glucans synthesized in pellicle. Inhibition studies with various polysaccharides and fungal dextranase indicated that alpha 1,6-linked glucose residues were of primary importance in the glucan binding observed. Scanning electron microscopic analysis showed direct binding of S. mutans to hydroxyapatite surface-associated polysaccharide and revealed no evidence of trapping or cell-to-cell binding. S. mutans strains also attached to host-derived structures in experimental pellicles, and the data suggest that the bacterial adhesins which recognize salivary binding sites were distinct from glucan-binding adhesins. Furthermore, glucans formed in experimental pellicles appeared to mask the host-derived components. These results support the concept that glucans synthesized in salivary pellicle can promote the selective adherence of the cariogenic streptococci which colonize human teeth.
机译:许多研究人员认为,葡聚糖介导的相互作用在变形链球菌粘附中的作用仅限于这种致龋细菌在其蔗糖(即葡聚糖)独立于唾液覆盖的牙齿表面结合后的积累。然而,唾液薄膜中存在酶促活性的葡糖基转移酶表明,葡聚糖还可以促进变形链球菌对牙齿的最初粘附。在本研究中,对常用的羟基磷灰石粘附试验进行了修改,以包括掺入葡萄糖基转移酶和在唾液包覆的羟基磷灰石珠子上原位合成葡聚糖。检查了变形链球菌的几种实验室菌株和临床分离株在有或没有事先就地形成葡聚糖的情况下粘附于实验薄膜的能力。结果表明,大多数变形链球菌菌株与表皮中合成的葡聚糖立体定向结合。用各种多糖和真菌葡聚糖酶进行的抑制研究表明,α1,6-连接的葡萄糖残基在观察到的葡聚糖结合中至关重要。扫描电子显微镜分析显示变形链球菌与羟基磷灰石表面相关多糖直接结合,并且没有捕获或细胞间结合的迹象。变形链球菌菌株也附着在实验薄膜的宿主衍生结构上,数据表明识别唾液结合位点的细菌粘附素不同于结合葡聚糖的粘附素。此外,在实验薄膜中形成的葡聚糖似乎掩盖了宿主来源的成分。这些结果支持在唾液薄膜中合成的葡聚糖可以促进定居人类牙齿的致龋链球菌的选择性粘附的概念。

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