Streptococcal glucosyltransferases (Gtf) synthesize α-glucan exopolymers which contribute to biofilm matrix. Streptococcus oralis interacts with the opportunistic pathogen Candida albicans to form hypervirulent biofilms. S. oralis 34 has a single gtf gene (gtfR). However, the role of gtfR in single and mixed species biofilms with C. albicans has never been examined. A gtfR deletion mutant, purified GtfR, and recombinant GtfR glucan-binding domain were tested in single and mixed biofilms on different substrata in vitro. A mouse oral infection model was also used. We found that in single species biofilms growing with sucrose on abiotic surfaces S. oralis gtfR increased biofilm matrix, but not bacterial biomass. In biofilms with C. albicans, S. oralis encoding gtfR showed increased bacterial biomass on all surfaces. C. albicans had a positive effect on α-glucan synthesis, and α-glucans increased C. albicans accretion on abiotic surfaces. In single and mixed infection of mice receiving sucrose S. oralis gtfR enhanced mucosal burdens. However, sucrose had a negative impact on C. albicans burdens and reduced S. oralis burdens in co-infected mice. Our data provide new insights on the GtfR-mediated interactions between the two organisms and the influence of biofilm substratum and the mucosal environment on these interactions.

中文翻译：

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葡萄糖基转移酶R在口腔链球菌和白色念珠菌之间的生物膜相互作用中的作用。

链球菌葡萄糖基转移酶（Gtf）合成有助于生物膜基质的α-葡聚糖外聚合物。口腔链球菌与机会病原体白色念珠菌相互作用，形成高毒性生物膜。口腔链球菌34具有单个gtf基因（gtfR）。但是，从未研究过gtfR在带有白色念珠菌的单一和混合物种生物膜中的作用。体外在不同基质上的单个和混合生物膜中测试了gtfR缺失突变体，纯化的GtfR和重组GtfR葡聚糖结合结构域。还使用了小鼠口腔感染模型。我们发现，在单种生物膜中，蔗糖在非生物表面上生长有蔗糖，S。oralis gtfR增加了生物膜基质，但没有增加细菌生物量。在带有白色念珠菌的生物膜中，编码gtfR的口腔链球菌在所有表面上均显示细菌生物量增加。C。白色念珠菌对α-葡聚糖的合成具有积极作用，并且α-葡聚糖增加了非生物表面上白色念珠菌的积聚。在接受蔗糖口腔链球菌gtfR的小鼠的单次和混合感染中，粘膜负担增加。然而，蔗糖对白色念珠菌的负担有负面影响，并减少了共感染小鼠的口头链球菌的负担。我们的数据为两种生物之间的GtfR介导的相互作用以及生物膜基质和粘膜环境对这些相互作用的影响提供了新的见解。