Ellen R P, Veisman H, Buivids I A, Rosenberg M
Faculty of Dentistry, University of Toronto, Ontario, Canada.
Oral Microbiol Immunol. 1994 Dec;9(6):364-71. doi: 10.1111/j.1399-302x.1994.tb00287.x.
Most investigations of mechanisms accounting for intergeneric coaggregation have emphasized stereospecific rather than nonspecific interactions. The purpose of this investigation was to determine the relative importance of lectin-carbohydrate and nonspecific hydrophobic and ionic interactions, using a model based on strains with one of the most well understood specific coaggregation mechanisms, the lactose-reversible coaggregation of Actinomyces naeslundii and Streptococcus oralis. The kinetics of coadhesion and desorption of coadherent bacteria were studied using S. oralis 34 bound to hexadecane droplets as an affinity support for the adhesion of A. naeslundii WVU 398A. Light, confocal microscopy and transmission electron microscopy confirmed that A. naeslundii cells adhered only to the S. oralis cells, not to exposed hexadecane between the streptococci. Coadhesion was inhibited by lactose concentrations as low as 2.0 mM. The rate of coadhesion was halved at 60 mM lactose. The hydrophobicity inhibitors bovine serum albumin and defatted bovine serum albumin and the salts LiCl and KCl failed to inhibit coadhesion in the hexadecane assay, and bovine serum albumin also failed to inhibit coaggregation in a bacterial aggregation assay on glass slides. High concentrations of the salts achieved a 50% rate decrease in A. naeslundii adhesion to the S. oralis-coated droplets only when they were combined with > 20 mM lactose. Sodium dodecyl sulfate (SDS) and Tween 20 inhibition was tested by the slide coaggregation assay because they tended to emulsify the droplets; SDS was inhibitory. Lactose selectively desorbed A. naeslundii from S. oralis-coated droplets at low concentrations equivalent to those that inhibited coadhesion. Neither LiCl nor KCl desorbed A. naeslundii from the droplets, even at 500 mM. At low concentrations, SDS but not Tween 20 eluted both A. naeslundii and S. oralis from the droplets. Although the SDS results might suggest a degree of cooperative charge interactions, the results support the hypothesis that stereospecific, beta-galactoside-sensitive interactions have a much greater impact than nonspecific interactions on the coadhesion of A. naeslundii and S. oralis.
大多数关于属间共聚集机制的研究都强调立体特异性相互作用而非非特异性相互作用。本研究的目的是利用一个基于具有最被深入理解的特定共聚集机制之一的菌株的模型，即内氏放线菌和口腔链球菌的乳糖可逆共聚集，来确定凝集素 - 碳水化合物以及非特异性疏水和离子相互作用的相对重要性。使用结合到十六烷液滴上的口腔链球菌34作为内氏放线菌WVU 398A黏附的亲和支持物，研究了共黏附细菌的共黏附和解吸动力学。光学显微镜、共聚焦显微镜和透射电子显微镜证实，内氏放线菌细胞仅黏附于口腔链球菌细胞，而非链球菌之间暴露的十六烷。低至2.0 mM的乳糖浓度即可抑制共黏附。在60 mM乳糖时，共黏附速率减半。疏水性抑制剂牛血清白蛋白和脱脂牛血清白蛋白以及盐LiCl和KCl在十六烷测定中未能抑制共黏附，并且牛血清白蛋白在载玻片上的细菌聚集测定中也未能抑制共聚集。仅当高浓度的盐与> 20 mM乳糖联合使用时，它们才使内氏放线菌对口腔链球菌包被液滴的黏附速率降低50%。通过载玻片共聚集测定测试了十二烷基硫酸钠（SDS）和吐温20的抑制作用，因为它们倾向于使液滴乳化；SDS具有抑制作用。乳糖在与抑制共黏附相同的低浓度下选择性地将内氏放线菌从口腔链球菌包被的液滴上解吸下来。即使在500 mM时，LiCl和KCl都不能从液滴上解吸内氏放线菌。在低浓度下，SDS而非吐温20从液滴上洗脱了内氏放线菌和口腔链球菌。尽管SDS的结果可能表明存在一定程度的协同电荷相互作用，但结果支持这样的假设，即立体特异性的、β - 半乳糖苷敏感的相互作用对内氏放线菌和口腔链球菌的共黏附的影响比非特异性相互作用大得多。
