Department of Oral Biology, University at Buffalo, Buffalo, New York, United States
Department of Oral Biology, University at Buffalo, Buffalo, New York, United States.
Appl Environ Microbiol. 2017 Dec 15;84(1). doi: 10.1128/AEM.01759-17. Print 2018 Jan 1.
and are dental plaque bacteria implicated in the development of periodontitis. These two species have been shown to form synergistic biofilms and have been found to be closely associated in dental plaque biofilms. A number of genetic loci for TonB-dependent membrane receptors (TDR) for glycan acquisition, with many existing in association with genes coding for enzymes involved in the breakdown of complex glycans, have been identified in In this study, we focused on a locus, BFO_0186-BFO_0188, that codes for a predicted TDR-SusD transporter along with a putative β-glucan hydrolyzing enzyme (BFO_0186). This operon is located immediately downstream of a 2-gene operon that codes for a putative stress-responsive extracytoplasmic function (ECF) sigma factor and an anti-sigma factor. Here, we show that BFO_0186 expresses a β-glucanase that cleaves glucans with β-1,6 and β-1,3 linkages. Furthermore, the BFO_0186-BFO_0188 locus is upregulated, with an induction of β-glucanase activity, in cobiofilms of and The β-glucanase activity in mixed biofilms in turn leads to an enhanced hydrolysis of β-glucans and release of glucose monomers and oligomers as nutrients for In summary, our study highlights the role of β-glucanase expressed by the asaccharolytic oral bacterium in the development of mixed species biofilms, and suggest that dietary β-glucans might contribute in plaque development and periodontal disease pathogenesis. The development of dental plaque biofilm is a complex process in which metabolic, chemical and physical interactions between bacteria take a central role. Previous studies have shown that the dental pathogens and form synergistic biofilms and are closely associated in human dental plaque. In this study, we show that β-glucanase from the periodontal pathogen plays a role in the formation of - cobiofilms by hydrolyzing β-glucans to glucose as a nutrient. We also unveiled that the expression of β-glucanase is induced in response to sensing. This study highlights the involvement of β-glucanase activity in the development of biofilms and suggests that intake of dietary β-glucans might be a contributing risk factor in plaque development and periodontal disease pathogenesis.
和 是与牙周炎发展有关的牙菌斑细菌。这两种细菌已被证明能形成协同生物膜，并在牙菌斑生物膜中密切相关。已经在 中鉴定出许多与糖获取的 TonB 依赖性膜受体 (TDR) 相关的遗传基因座，其中许多与编码参与复杂糖分解的酶的基因相关。在这项研究中，我们专注于一个基因座 BFO_0186-BFO_0188，该基因座编码预测的 TDR-SusD 转运蛋白以及假定的 β-葡聚糖水解酶 (BFO_0186)。该操纵子位于编码假定应激反应细胞外功能 (ECF) σ因子和抗σ因子的 2 基因操纵子的下游。在这里，我们表明 BFO_0186 表达一种 β-葡聚糖酶，可切割具有 β-1,6 和 β-1,3 键的葡聚糖。此外，BFO_0186-BFO_0188 基因座上调，β-葡聚糖酶活性诱导， 和 的共生物膜中。混合生物膜中的 β-葡聚糖酶活性进而导致 β-葡聚糖的水解增强，并释放葡萄糖单体和低聚物作为 的营养物质。总之，我们的研究强调了口腔细菌 中 β-葡聚糖酶在 混合物种生物膜发展中的作用，并表明饮食中的 β-葡聚糖可能有助于菌斑形成和牙周病发病机制。牙菌斑生物膜的发展是一个复杂的过程，其中细菌之间的代谢、化学和物理相互作用起着核心作用。先前的研究表明，口腔病原体 和 形成协同生物膜，并在人类牙菌斑中密切相关。在这项研究中，我们表明牙周病原体 的 β-葡聚糖酶通过水解 β-葡聚糖产生葡萄糖作为营养物质在 - 共生物膜的形成中起作用。我们还揭示了对 的感知会诱导 β-葡聚糖酶的表达。这项研究强调了 β-葡聚糖酶活性在生物膜发展中的作用，并表明饮食中 β-葡聚糖的摄入可能是菌斑形成和牙周病发病机制的一个促成风险因素。
