Weinberg A, Holt S C
Department of Periodontics, University of Texas Health Science Center, San Antonio 78284-7894.
Infect Immun. 1990 Jun;58(6):1720-9. doi: 10.1128/iai.58.6.1720-1729.1990.
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.
研究了具核梭杆菌GM-1、TD-4和MS25对人牙龈成纤维细胞(HGFs)的黏附情况,以此作为研究这些口腔细菌与人类宿主细胞相互作用的开端。在需氧(5%二氧化碳)和厌氧(85%氮气加10%氢气加5%二氧化碳)环境下,GM-1和MS25菌株与HGFs的相互作用表明,它们始终比TD-4菌株更具黏附性。针对GM-1的多克隆抗体可使GM-1的黏附性降低70%,而MS25和TD-4表现出不同程度的交叉反应抑制,这表明三种具核梭杆菌菌株表面存在共同但不完全相同的表位。用胰蛋白酶预处理这三种菌株并未抑制黏附;然而,蛋白酶K可使这种相互作用降低80%。用胰蛋白酶预处理HGFs后,GM-1和MS25的黏附性分别增加了50%和86%,而TD-4的黏附性则下降了41%。将具核梭杆菌菌株暴露于糖类以及对HGFs进行凝集素预处理表明,HGFs表面的甘露糖和半乳糖残基参与了黏附介导过程。用高碘酸盐处理HGFs后,GM-1和MS25的黏附性下降了50%,但TD-4的黏附性并未降低。添加胎牛血清会不同程度地抑制这三种菌株的黏附,其中TD-4最为敏感。添加纯化的纤连蛋白(100微克/毫升)可使GM-1和MS25的黏附性抑制率超过50%,而TD-4的黏附性则增加了25%。虽然在所研究的一些参数中发现了菌株差异,但结果表明具核梭杆菌与HGFs黏附存在两种可能性:具核梭杆菌表面存在一种对HGFs表面的半乳糖和甘露糖具有亲和力的类凝集素黏附素,以及一种连接具核梭杆菌和HGFs的血清宿主因子。