van Hoogmoed C G, van Der Kuijl-Booij M, van Der Mei H C, Busscher H J
Department of Biomedical Engineering, University of Groningen, 9712 KZ Groningen, The Netherlands.
Appl Environ Microbiol. 2000 Feb;66(2):659-63. doi: 10.1128/AEM.66.2.659-663.2000.
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.
此前已有研究报道，在泌尿生殖道、肠道和口咽部，益生菌可通过分泌生物表面活性剂来抵御同一基质表面上其他定殖菌株，然而口腔微生物的此类现象尚未见报道。两株缓症链球菌（BA和BMS）在蔗糖存在的条件下生长，并在稳定期早期收获时，释放出最大量的生物表面活性剂。缓症链球菌生物表面活性剂可将水溶液的表面张力降低至约30至40 mJ m(-2)。生化和物理化学分析表明，释放出的生物表面活性剂为糖脂。酸沉淀部分具有极强的表面活性，被鉴定为类鼠李糖脂化合物。在平行平板流动腔中，与不存在缓症链球菌时相比，在分泌生物表面活性剂的缓症链球菌BA和BMS（表面覆盖率为1%至4%）存在的情况下，变形链球菌NS细胞在有和没有唾液调节膜的玻璃上的黏附数量显著减少。在不存在生物表面活性剂分泌型缓症链球菌BA和BMS的情况下，变形链球菌NS的黏附完全没有减少。此外，将分离出的缓症链球菌生物表面活性剂预吸附到玻璃上，可显著降低变形链球菌NS细胞的黏附及其与玻璃结合的强度，如通过气泡通过流动腔使变形链球菌NS细胞脱落的百分比增加所示。酸沉淀部分的预吸附以剂量反应方式抑制变形链球菌黏附达80%。这些观察结果表明，缓症链球菌在口腔中发挥保护作用，可防止致龋性变形链球菌在唾液包被的表面定殖。
