MECHANISM OF CO-AGGREGATION BETWEEN ACTINOMYCES-VISCOSUS T14V AND STREPTOCOCCUS-SANGUIS-34
MECHANISM OF CO-AGGREGATION BETWEEN ACTINOMYCES-VISCOSUS T14V AND STREPTOCOCCUS-SANGUIS-34
复制标题
DOI：
10.1128/iai.21.3.978-988.1978
复制
发表时间：
1978-01-01
影响因子：
3.1
通讯作者：
ARNOLD, J
中科院分区：
文献类型：
--
作者：
MCINTIRE, FC;VATTER, AE;ARNOLD, J
A. viscous T14V 和 S. sanguis 34 通过不受 1 M NaCl 抑制的机制共聚集，不依赖于葡聚糖，需要 Ca，pH 依赖性，最适 pH 为 8.0-8.5，并且似乎需要 A. viscosus 上的蛋白质或糖蛋白与 S. sanguis 上的碳水化合物相互作用。 0.01M乳糖、0.02Mβ-甲基-D-半乳糖苷或0.05MD-半乳糖抑制共聚集超过80%；在0.1Mα-甲基-D-半乳糖苷、蜜二糖、麦芽糖、纤维二糖、蔗糖和许多单糖中，共聚集的抑制小于10％。在酶浓度非常高的情况下，灰色链霉菌的蛋白酶破坏了粘性链霉菌上的反应位点，但没有破坏安氏链霉菌上的反应位点。两者都对葡聚糖酶完全耐药。高碘酸盐（0.01 M；pH 4）可使两种细菌失活。 65℃的苯酚-水提取不会破坏血链球菌与粘性血球菌共聚集的能力。 C 15 分钟。当细菌在特定条件下培养时，共聚集具有高度可重复性。在相同条件下，T14AV（粘性曲霉 T14V 的无毒突变体）不与血链球菌 34 共聚集。用粘性曲霉抗体对共聚集物进行免疫化学标记的电镜研究表明，粘性曲霉上的原纤维可能参与了共聚集。 [这些发现与牙菌斑的形成有关]。
A. viscosus T14V and S. sanguis 34 coaggregate by a mechanism which is not inhibited by 1 M NaCl, is dextran independent, requires Ca, is pH dependent with an optimum at pH 8.0-8.5 and appears to require the interaction of a protein or glycoprotein on A. viscosus with a carbohydrate on S. sanguis. The coaggregation is inhibited more than 80% by 0.01 M lactose, 0.02 M .beta.-methyl-D-galactoside or 0.05 M D-galactose; inhibition of coaggregation was less than 10% in 0.1 M .alpha.-methyl-D-galactoside, melibiose, maltose, cellobiose, sucrose and a number of monosaccharides. At very high concentrations of enzyme, protease from Streptomyces griseus destroyed the reactive site on A. viscosus but not on S. ansguis. Both were totally resistant to dextranase. Periodate (0.01 M; pH 4) inactivated both bacteria. The ability of S. sanguis to coaggregate with A. viscosus was not destroyed by phenol-water extraction at 65.degree. C for 15 min. When the bacteria were cultured under specified conditions, the coaggregation was highly reproducible. Under the same conditions, T14AV, the avirulent mutant of A. viscosus T14V, did not coaggregate with S. sanguis 34. EM studies of coaggregates, labeled immunochemically with antibody to A. viscosus, indicated that fibrils on A. viscosus may be involved in the coaggregation. [These findings have relevance to dental plaque formation.].