Department of Oral Microbiology, Faculty of Dentistry, Mahidol University, Bangkok, 10400, Thailand.
Department of Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, 700-8525, Japan.
Arch Oral Biol. 2017 Sep;81:7-14. doi: 10.1016/j.archoralbio.2017.04.018. Epub 2017 Apr 21.
In Streptococcus mutans, a Gram-positive pathogen of dental caries, several surface proteins are anchored by the activity of sortase enzyme. Although various reports have shown that constructed S. mutans mutants deficient of sortase as well as laboratory reference strains with a sortase gene mutation have low cariogenic potential, no known studies have investigated clinical isolates with sortase defects. Here, we examined the cariogenic properties of S. mutans clinical isolates with sortase defects as well as caries status in humans harboring such defective isolates.
Sortase-defective clinical isolates were evaluated for biofilm formation, sucrose-dependent adhesion, stress-induced dextran-dependent aggregation, acid production, and acid tolerance. Additionally, caries indices of subjects possessing such defective isolates were determined.
Our in vitro results indicated that biofilm with a lower quantity was formed by sortase-defective as compared to non-defective isolates. Moreover, impairments of sucrose-dependent adhesion and stress-induced dextran-dependent aggregation were found among the isolates with defects, whereas no alterations were seen in regard to acid production or tolerance. Furthermore, glucan-binding protein C, a surface protein anchored by sortase activity, was predominantly detected in culture supernatants of all sortase-defective S. mutans isolates. Although the sortase-defective isolates showed lower cariogenic potential because of a reduction in some cariogenic properties, deft/DMFT indices revealed that all subjects harboring those isolates had caries experience.
Our findings suggest the impairment of cariogenic properties in S. mutans clinical isolates with sortase defects, though the detection of these defective isolates seemed not to imply low caries risk in the subjects harboring them.
在致龋性革兰阳性菌变形链球菌中，多种表面蛋白通过天冬酰胺酰基内肽酶（sortase）的活性锚定。虽然已有多项研究表明，构建的天冬酰胺酰基内肽酶缺陷型变形链球菌突变株和具有天冬酰胺酰基内肽酶基因突变的实验室参考株的致龋性较低，但尚未有研究调查具有天冬酰胺酰基内肽酶缺陷的临床分离株。本研究旨在检测具有天冬酰胺酰基内肽酶缺陷的变形链球菌临床分离株的致龋特性以及携带此类缺陷分离株的个体的龋病状况。
评估天冬酰胺酰基内肽酶缺陷的临床分离株的生物膜形成、蔗糖依赖性黏附、应激诱导的葡聚糖依赖性聚集、产酸和酸耐受能力。此外，还确定了携带此类缺陷分离株的个体的龋病指数。
我们的体外研究结果表明，与非缺陷型分离株相比，天冬酰胺酰基内肽酶缺陷型分离株形成的生物膜数量较少。此外，缺陷型分离株存在蔗糖依赖性黏附受损和应激诱导的葡聚糖依赖性聚集受损，但在产酸或耐酸方面未见改变。此外，葡聚糖结合蛋白 C（一种由天冬酰胺酰基内肽酶活性锚定的表面蛋白）主要在所有天冬酰胺酰基内肽酶缺陷型变形链球菌分离株的培养上清液中检测到。虽然由于一些致龋特性的降低，天冬酰胺酰基内肽酶缺陷型分离株的致龋潜力降低，但缺牙数/失牙数/充填牙数（dmft）指数表明，所有携带这些分离株的个体都有龋病经历。
我们的研究结果表明，天冬酰胺酰基内肽酶缺陷的变形链球菌临床分离株的致龋特性受损，尽管检测到这些缺陷分离株似乎并不意味着携带这些分离株的个体龋病风险较低。
