Steinberg D, Kopec L K, Bowen W H
Department of Dental Research, Rochester Caries Research Center, University of Rochester, New York 14642.
J Dent Res. 1993 Jun;72(6):1015-20. doi: 10.1177/00220345930720060401.
The ability of oral bacteria to adhere to surfaces is associated with their pathogenicity. Actinomyces can adhere to pellicle and cells through extracellular fimbriae. Research on adhesion of actinomyces has been conducted with use of hydroxyapatite (HA) coated with mammalian-derived salivary constituents, whereas the bacterial-derived components of the acquired pellicle have been largely ignored. The influence of the cell-free bacterial enzyme, glucosyltransferase (GTF), on adhesion of human and rodent isolates of Actinomyces viscosus was examined. Cell-free GTF was adsorbed onto parotid saliva-coated hydroxyapatite (sHA). Next, A. viscosus was exposed to the pellicle following the synthesis of glucan formed in situ by GTF. Glucans formed on the pellicle served as binding sites for adhesion of a rodent strain of A. viscosus. Conversely, the presence of in situ glucans on sHA reduced the adhesion of human isolates of A. viscosus compared with their adhesion to sHA. Adhesion of the rodent strains may be facilitated through a dextran-binding protein, since the rodent strains aggregated in the presence of dextrans and mutan. The human isolates were not aggregated by dextran or mutan. Pellicle harboring A. viscosus rodent strains interfered with the subsequent adhesion of Streptococcus mutans to the bacterial-coated pellicle. In contrast, the adhesion of S. mutans to pellicle was not decreased when the pellicle was pre-exposed to a human isolate of A. viscosus. The experimental data suggest that human and the rodent isolates of A. viscosus have distinct glucan adhesion properties.(ABSTRACT TRUNCATED AT 250 WORDS)
口腔细菌黏附于表面的能力与其致病性相关。放线菌可通过细胞外菌毛黏附于获得性膜和细胞。关于放线菌黏附的研究是利用涂有哺乳动物来源唾液成分的羟基磷灰石（HA）进行的，而获得性膜中细菌来源的成分在很大程度上被忽视了。研究了无细胞细菌酶葡糖基转移酶（GTF）对人源和啮齿动物源黏性放线菌黏附的影响。无细胞GTF吸附在腮腺唾液包被的羟基磷灰石（sHA）上。接下来，在GTF原位合成葡聚糖后，将黏性放线菌暴露于获得性膜。在获得性膜上形成的葡聚糖作为啮齿动物源黏性放线菌菌株黏附的结合位点。相反，与黏性放线菌人源菌株黏附于sHA相比，sHA上原位葡聚糖的存在降低了其黏附。啮齿动物源菌株的黏附可能通过一种葡聚糖结合蛋白促进，因为啮齿动物源菌株在葡聚糖和变聚糖存在时会聚集。人源菌株不会被葡聚糖或变聚糖聚集。携带啮齿动物源黏性放线菌菌株的获得性膜会干扰变形链球菌随后对细菌包被的获得性膜的黏附。相比之下，当获得性膜预先暴露于人源黏性放线菌时，变形链球菌对获得性膜的黏附并未降低。实验数据表明，人源和啮齿动物源黏性放线菌具有不同的葡聚糖黏附特性。（摘要截短于250字）
