Staat R H, Langley S D, Doyle R J
Infect Immun. 1980 Feb;27(2):675-81. doi: 10.1128/iai.27.2.675-681.1980.
Adherence of Streptococcus mutans to smooth surfaces has been attributed to the production of sucrose-derived d-glucans. However, several studies indicate that the bacterium will adhere in the absence of sucrose. The present data confirmed that S. mutans adherence to saliva-coated hydroxyapatite beads in the absence of sucrose is described by the Langmuir equation. The nature of the sucrose-independent adherence was studied with the Persea americana agglutinin as a selective adherence inhibitor. Pretreatment of the bacterium with P. americana agglutinin caused a 10-fold reduction in adherence, and the inhibition was not reversed with the addition of sucrose. Pretreatment of S. mutans with proteases also reduced adherence, regardless of the sucrose content, whereas periodate oxidation and glucanohydrolase treatment of the bacteria reduced sucrose-mediated adherence to the levels found for sucrose-independent adherence. The P. americana agglutinin, glucanohydrolase, and pepsin pretreatment of the cells did not eliminate sucrose-induced agglutination. Scanning electron microscopy showed that short streptococcal chains were bound to saliva-coated hydroxyapatite crystals in the sucrose-independent system, whereas the presence of sucrose caused larger bacterial clumps to be found. A two-reaction model of S. mutans adherence was developed from these data. It is proposed that one reaction is attachment to the tooth pellicle which is mediated by cell-surface proteins rather than glucans or teichoic acids. The other reaction is cellular accumulation mediated by sucrose-derived d-glucans and cell surface lectins. A series of sequential adherence experiments with P. americana agglutinin as a selective inhibitor provided presumptive evidence for the validity of our model of S. mutans adherence.
变形链球菌对光滑表面的黏附归因于蔗糖衍生的d-葡聚糖的产生。然而，多项研究表明，该细菌在没有蔗糖的情况下也会黏附。目前的数据证实，在没有蔗糖的情况下，变形链球菌对唾液包被的羟基磷灰石珠的黏附可用朗缪尔方程来描述。以鳄梨凝集素作为选择性黏附抑制剂，研究了不依赖蔗糖的黏附的性质。用鳄梨凝集素对细菌进行预处理可使黏附减少10倍，且添加蔗糖并不能逆转这种抑制作用。用蛋白酶对变形链球菌进行预处理也会降低黏附，而与蔗糖含量无关，而对细菌进行高碘酸盐氧化和葡聚糖水解酶处理则会使蔗糖介导的黏附降低到不依赖蔗糖的黏附水平。对细胞进行鳄梨凝集素、葡聚糖水解酶和胃蛋白酶预处理并不能消除蔗糖诱导的凝集。扫描电子显微镜显示，在不依赖蔗糖的系统中，短链链球菌与唾液包被的羟基磷灰石晶体结合，而在有蔗糖存在的情况下，则会发现更大的细菌团块。根据这些数据建立了变形链球菌黏附的双反应模型。有人提出，一种反应是通过细胞表面蛋白而非葡聚糖或磷壁酸介导的与牙菌斑的附着。另一种反应是由蔗糖衍生的d-葡聚糖和细胞表面凝集素介导的细胞聚集。以鳄梨凝集素作为选择性抑制剂进行的一系列连续黏附实验为我们的变形链球菌黏附模型的有效性提供了初步证据。
