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Deficiency of BrpA in Streptococcus mutans reduces virulence in rat caries model.
Molecular Oral Microbiology ( IF 2.8 ) Pub Date : 2018-07-17 , DOI: 10.1111/omi.12230
Zezhang T Wen 1, 2, 3 , Kathleen Scott-Anne 4 , Sumei Liao 2 , Arpan De 1 , Meng Luo 3 , Christopher Kovacs 4 , Brendaliz S Narvaez 4 , Roberta C Faustoferri 4 , Qingzhao Yu 5 , Christopher M Taylor 3 , Robert G Quivey 4
Affiliation  

Our recent studies have shown that BrpA in Streptococcus mutans plays a critical role in cell envelope biogenesis, stress responses, and biofilm formation. In this study, a 10‐species consortium was used to assess how BrpA deficiency influences the establishment, persistence, and competitiveness of S. mutans during growth in a community under conditions typical of the oral cavity. Results showed that, like the wild‐type, the brpA mutant was able to colonize and establish on the surfaces tested. Relative to the wild‐type, however, the brpA mutant had a reduced ability to persist and grow in the 10‐species consortium (< .001). A rat caries model was also used to examine the effect of BrpA, as well as Psr, a BrpA paralog, on S. mutans cariogenicity. The results showed no major differences in infectivity between the wild‐type and the brpA and psr mutants. Unlike the wild‐type, however, infection with the brpA mutant, but not the psr mutant, showed no significant differences in both total numbers of carious lesions and caries severity, compared with the control group that received bacterial growth medium (> .05). Metagenomic and quantitative polymerase chain reaction analysis showed that S. mutans infection caused major alterations in the composition of the rats’ plaque microbiota and that significantly less S. mutans was identified in the rats infected with the brpA mutant compared with those infected with the wild‐type and the psr mutant. These results further suggest that BrpA plays a critical role in S. mutans pathophysiology and that BrpA has potential as a therapeutic target in the modulation of S. mutans virulence.

中文翻译:


变形链球菌中 BrpA 的缺乏会降低大鼠龋齿模型中的毒力。



我们最近的研究表明,变形链球菌中的 BrpA 在细胞包膜生物发生、应激反应和生物膜形成中发挥着关键作用。在本研究中,使用 10 个物种的联合体来评估 BrpA 缺陷如何影响变形链球菌在典型口腔条件下群落生长过程中的建立、持久性和竞争力。结果表明,与野生型一样, brpA突变体能够在测试的表面上定殖并建立。然而,相对于野生型, brpA突变体在 10 种联合体中持续存在和生长的能力较低 ( P < .001)。还使用大鼠龋齿模型来检查 BrpA 以及 Psr(BrpA 旁系同源物)对变形链球菌致龋性的影响。结果显示野生型与brpApsr突变体之间的感染性没有重大差异。然而,与野生型不同的是,与接受细菌生长培养基的对照组相比,感染brpA突变体(而非psr突变体)在龋损总数和龋齿严重程度方面均没有显着差异( P > .05 )。宏基因组和定量聚合酶链反应分析表明,变形链球菌感染导致大鼠斑块微生物群的组成发生重大变化,并且与感染野生型的大鼠相比,感染brpA突变体的大鼠中发现的变形链球菌数量显着减少。型和psr突变体。这些结果进一步表明 BrpA 在S.变形链球菌病理生理学,并且 BrpA 有潜力作为调节变形链球菌毒力的治疗靶点。
更新日期:2018-07-17
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