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Inhibition of Streptococcus mutans NS Adhesion to Glass with and without a Salivary Conditioning Film by Biosurfactant- Releasing Streptococcus mitis Strains

机译:含和不含唾液调理膜的变形链球菌NS粘附对释放生物表面活性剂的链球菌微生物菌株的抑制作用

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摘要

The release of biosurfactants by adhering microorganisms as a defense mechanism against other colonizing strains on the same substratum surface has been described previously for probiotic bacteria in the urogenital tract, the intestines, and the oropharynx but not for microorganisms in the oral cavity. Two Streptococcus mitis strains (BA and BMS) released maximal amounts of biosurfactants when they were grown in the presence of sucrose and were harvested in the early stationary phase. The S. mitis biosurfactants reduced the surface tensions of aqueous solutions to about 30 to 40 mJ m−2. Biochemical and physicochemical analyses revealed that the biosurfactants released were glycolipids. An acid-precipitated fraction was extremely surfactive and was identified as a rhamnolipidlike compound. In a parallel-plate flow chamber, the number of Streptococcus mutans NS cells adhering to glass with and without a salivary conditioning film in the presence of biosurfactant-releasing S. mitis BA and BMS (surface coverage, 1 to 4%) was significantly reduced compared with the number of S. mutans NS cells adhering to glass in the absence of S. mitis. S. mutans NS adhesion in the presence of non-biosurfactant-releasing S. mitis BA and BMS was not reduced at all. In addition, preadsorption of isolated S. mitis biosurfactants to glass drastically reduced the adhesion of S. mutans NS cells and the strength of their bonds to glass, as shown by the increased percentage of S. mutans NS cells detached by the passage of air bubbles through the flow chamber. Preadsorption of the acid-precipitated fraction inhibited S. mutans adhesion up to 80% in a dose-responsive manner. These observations indicate that S. mitis plays a protective role in the oral cavity and protects against colonization of saliva-coated surfaces by cariogenic S. mutans.
机译:先前已经针对泌尿生殖道,肠和口咽中的益生菌而非口腔中的微生物描述了通过粘附微生物而释放生物表面活性剂,以作为针对同一基质表面上其他定殖菌株的防御机制。当两种链球菌的微生物菌株(BA和BMS)在蔗糖存在下生长并在静止早期收获时,释放出最大量的生物表面活性剂。微生物链霉菌生物表面活性剂将水溶液的表面张力降低至约30至40 mJ m -2 。生化和理化分析表明,释放的生物表面活性剂是糖脂。酸沉淀的馏分具有极强的表面活性,被鉴定为鼠李糖脂样化合物。在平行板流动室中,在存在或不存在唾液调节膜的情况下,在存在生物表面活性剂释放链球菌BA和BMS的情况下,粘附在玻璃上的变形链球菌NS细胞数量明显减少(表面覆盖率1-4%)与在没有链球菌的情况下粘附在玻璃上的变形链球菌NS细胞的数量进行比较。在不释放生物表面活性剂的链球菌BA和BMS的情况下,变形链球菌的NS粘附力完全没有降低。另外,分离的链球菌生物表面活性剂对玻璃的预吸附极大地降低了变形链球菌NS细胞的粘附力和它们与玻璃的结合强度,如通过气泡通过而分离的变形链球菌NS细胞的百分比增加所示。通过流动室。酸沉淀级分的预先吸附以剂量响应方式将变形链球菌粘附抑制高达80%。这些观察结果表明,链球菌在口腔中起保护作用,并防止由致龋性链球菌引起的唾液覆盖表面的定植。

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