Isolation and Bacteriocin-Related Typing of Streptococcus dentisani
Isolation and Bacteriocin-Related Typing of Streptococcus dentisani
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DOI：
10.3389/fcimb.2019.00110
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发表时间：
2019-04-16
影响因子：
5.7
通讯作者：
Abdelbary, Mohamed M. H.
中科院分区：
文献类型：
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作者：
Conrads, Georg;Westenberger, Jacqueline;Abdelbary, Mohamed M. H.
口腔链球菌亚种dentisani被探索为抗致龋益生菌。在这里，35名健康志愿者的新鲜刺激的唾液样本，6个流行病学无关和2个相关菌株分离（患病率约20%）应用新开发的三步程序。此外，益生菌菌株S.在多种环境条件下测试了Dentisani 7746（AB-Dentisanium（R））对六种S. mutans，两个S. sobrinus，其他口腔或肠道链球菌15株，链球菌15株。dentisani菌株和包括牙周病原体在内的其他物种的六个代表。除了一个S。7746菌落或培养物上清液浓缩物可抑制变形菌株，但仅当试验细胞数低或生产者或其细菌素浓度分别高时。S. sanguinis OMI 332、S. salivarius OMI 315、S. parasanguinis OMI 335、S. vestibularis OMI 238和肠S.停乳链球菌OMI 339的抑乳作用不明显，而其它10株链球菌（尤其是S. oralis OMI 334和肠S. gallolyticus OMI 326）表现出一定程度的抑制作用。从其他细菌物种的面板只有Aggregatibacteractinomycetemcomitans轻微抑制。除OMI 285和OMI 291具有7746个细菌素样基因簇外，其余菌株均为S。7746对dentisani菌株，尤其是模式菌株7747（T）有较强的抑制作用。结论：益生菌7746可能通过减少S.如果不是太多的话S.牙病菌株相互抑制，但具有类似细菌素相关基因簇（包括免疫基因）的菌株由于交叉抗性而能够共存。此外，在我们的研究过程中观察到对7746-细菌素的抗性和适应性的发展，需要引起注意。因此，这些过程的机制需要进一步研究使用组学方法。在生产水平上，应持续测试益生菌菌株的功能。进一步的临床研究调查抑制S。需要AB-Dentisanium（R）的变形杆菌，还应监测对口腔微生物组组成的影响，包括常驻S。牙科菌株。
Streptococcus oralis subspecies dentisani is explored as an anti-cariogenic probiotic. Here, subjecting freshly stimulated saliva samples of 35 healthy volunteers, six epidemiologically unrelated and two related strains were isolated (prevalence around 20%) applying a newly developed three-step procedure. Furthermore, the probiotic strain S. dentisani 7746 (AB-Dentisanium (R)) was tested under a variety of environmental conditions for its inhibitory effect on six S. mutans, two S. sobrinus, 15 other oral or intestinal streptococci, 15 S. dentisani strains, and six representatives of other species including periodontopathogens. All except one of the S. mutans strains were inhibited by 7746 colonies or culture supernatant concentrate but only if either the test cell number was low or the producer or its bacteriocin concentration, respectively, was high. S. sanguinis OMI 332, S. salivarius OMI 315, S. parasanguinis OMI 335, S. vestibularis OMI 238, and the intestinal S. dysgalactiae OMI 339 were not inhibited, while the other 10 streptococcal strains (especially S. oralis OMI 334 and intestinal S. gallolyticus OMI 326) showed a certain degree of inhibition. From the panel of other bacterial species only Aggregatibacter actinomycetemcomitans was slightly inhibited. With the exception of OMI 285 and OMI 291 that possessed a 7746 bacteriocin-like gene cluster, all S. dentisani strains and especially type strain 7747(T) were strongly inhibited by 7746. In conclusion, probiotic strain 7746 might antagonize the initiation and progression of dental caries by reducing S. mutans if not too abundant. S. dentisani strains inhibit each other, but strains with similar bacteriocin-related gene clusters, including immunity genes, are able to co-exist due to cross-resistance. In addition, development of resistance and adaptation to 7746-bacteriocins was observed during our study and needs attention. Hence, mechanisms underlying such processes need to be further investigated using omics-approaches. On the manufacturing level, probiotic strains should be continuously tested for function. Further clinical studies investigating inhibition of S. mutans by AB-Dentisanium (R) are required that should also monitor the impact on the oral microbiome composition including resident S. dentisani strains.