The adherence of Treponema denticola GM-1, TD-4, and MS25 to human gingival fibroblasts (HGFs) was studied to serve as an introduction to investigations into the interactions of these oral bacteria with human host cells. Under both aerobic (5% CO2) and anaerobic (85% N2 plus 10% H2 plus 5% CO2) environments, the interactions with the HGFs were such that strains GM-1 and MS25 were consistently more adherent than strain TD-4. Polyclonal antibodies to GM-1 inhibited GM-1 adherence by 70%, while MS25 and TD-4 showed differing degrees of cross-reactive inhibition, indicative of common but not identical epitopes on the surface of the three T. denticola strains. Pretreatment of the three strains with trypsin did not inhibit adherence; proteinase K did, however, inhibit this interaction by 80%. Trypsin pretreatment of the HGFs resulted in increases in adherence of 50 and 86% for GM-1 and MS25, respectively, while a decrease of 41% was noted for TD-4. Exposure of the T. denticola strains to sugars and lectin pretreatment of the HGFs implicated adherence mediation by mannose and galactose residues on the HGF surface. Periodate treatment of HGFs resulted in a 50% drop in adherence for GM-1 and MS25, but did not decrease that of TD-4. Addition of fetal bovine serum inhibited adherence of the three strains to differing degrees, with TD-4 being the most susceptible. Addition of purified fibronectin (100 micrograms/ml) resulted in greater than 50% inhibition in GM-1 and MS25 adherence, while a 25% increase occurred with TD-4. While strain differences were noted in some of the parameters studied, the results indicate two possibilities for T. denticola-HGF adherence: a lectinlike adhesin(s) on the T. denticola surface with affinity for galactose and mannose on the HGF surface, and a serum host factor(s) bridging T. denticola and HGFs.
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机译:研究了密闭螺旋体GM-1,TD-4和MS25对人牙龈成纤维细胞(HGF)的粘附性,以作为研究这些口腔细菌与人宿主细胞相互作用的介绍。在有氧(5%CO2)和厌氧(85%N2加10%H2加5%CO2)环境下,与HGF的相互作用使得GM-1和MS25菌株的黏附力始终比TD-4菌株高。针对GM-1的多克隆抗体可将GM-1的粘附抑制70%,而MS25和TD-4则显示出不同程度的交叉反应抑制作用,表明这三种树突孢菌菌株表面存在共同但不相同的表位。用胰蛋白酶预处理这三株菌株不会抑制粘附。但是,蛋白酶K确实抑制了80%的相互作用。胰蛋白酶对HGF的预处理导致GM-1和MS25的依从性分别增加50%和86%,而TD-4的依从性下降41%。 T. denticola菌株暴露于糖和HGF的凝集素预处理涉及HGF表面的甘露糖和半乳糖残基的粘附介导。对HGF的定期治疗导致GM-1和MS25的依从性下降了50%,但并未降低TD-4的依从性。胎牛血清的添加在不同程度上抑制了三种菌株的粘附,其中TD-4是最易感的。添加纯化的纤连蛋白(100微克/毫升)可导致GM-1和MS25的粘附抑制超过50%,而TD-4则增加25%。虽然在某些研究参数中注意到了应变差异,但结果表明树突状细胞-HGF的粘附有两种可能性:树突状细胞表面上与半乳糖和甘露糖有亲和力的凝集素样粘附素,以及桥接T. denticola和HGF的血清宿主因子。
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