Streptococcus gordonii Hsa environmentally constrains competitive binding by Streptococcus sanguinis to saliva-coated hydroxyapatite

Streptococcus gordonii Hsa environmentally constrains competitive binding by Streptococcus sanguinis to saliva-coated hydroxyapatite
复制标题

DOI:
10.1128/jb.01535-06
复制
发表时间:
2007-04-01
影响因子:
3.2
通讯作者:
Herzberg, Mark C.
Herzberg, Mark C.
中科院分区:
生物学3区
文献类型:
--
作者:
Nobbs, Angela H.;Zhang, Yongshu;Herzberg, Mark C.

文献摘要

被引文献

相似文献

先锋定植细菌之间的竞争可能决定在牙菌斑的发展过程中的多微生物的继承,但生态限制知之甚少。例如,从同一口内部位分离的血链球菌比戈登链球菌多,而S。戈登氏鱼未能被排除在外,并作为一个物种随着时间的推移而生存下来。为了解释这一观察结果,我们假设S。gordonii可以与S. sanguinis粘附到唾液包被的羟基磷灰石(sHA),牙齿表面的体外模型。两种物质与sHA的结合相似,但S过量10至50倍。gordonii DL 1降低了S.血细胞SK 36的表达量增加85%至> 95%。S. sanguinis与S.戈登要坚持。S. gordonii与S.血链球菌对HA的敏感性高于其他口腔链球菌,且依赖于HA的唾液膜。其次,假设S。分析戈登氏菌粘附素对种间竞争结合的贡献。与野生型S. gordonii,抗原I/II多肽(sspAB)、淀粉酶结合蛋白(abpAB)和Csh粘附素(cshAB)突变的同基因突变体有效地竞争S.吸血鬼相比之下,S. Gordonii显示出显著降低的结合和竞争能力,而这些性质在HSA补充的菌株中得到恢复。因此,Hsa赋予S选择优势。gordonii优于S.血吸虫与sHA竞争性结合。因此,HSA表达可能作为针对S. sanguinis,使S. gordonii在口腔内持续存在,尽管S.牙菌斑和唾液中的血细胞。
Competition between pioneer colonizing bacteria may determine polymicrobial succession during dental plaque development, but the ecological constraints are poorly understood. For example, more Streptococcus sanguinis than Streptococcus gordonii organisms are consistently isolated from the same intraoral sites, yet S. gordonii fails to be excluded and survives as a species over time. To explain this observation, we hypothesized that S. gordonii could compete with S. sanguinis to adhere to saliva-coated hydroxyapatite (sHA), an in vitro model of the tooth surface. Both species bound similarly to sHA, yet 10- to 50-fold excess S. gordonii DL1 reduced binding of S. sanguinis SK36 by 85 to >95%. S. sanguinis, by contrast, did not significantly compete with S. gordonii to adhere. S. gordonii competed with S. sanguinis more effectively than other species of oral streptococci and depended upon the salivary film on HA. Next, putative S. gordonii adhesins were analyzed for contributions to interspecies competitive binding. Like wild-type S. gordonii, isogenic mutants with mutations in antigen I/II polypeptides (sspAB), amylase-binding proteins (abpAB), and Csh adhesins (cshAB) competed effectively against S. sanguinis. By contrast, an hsa-deficient mutant of S. gordonii showed significantly reduced binding and competitive capabilities, while these properties were restored in an hsa-complemented strain. Thus, Hsa confers a selective advantage to S. gordonii over S. sanguinis in competitive binding to sHA. Hsa expression may, therefore, serve as an environmental constraint against S. sanguinis, enabling S. gordonii to persist within the oral cavity, despite the greater natural prevalence of S. sanguinis in plaque and saliva.