D-Galactose as an autoinducer 2 inhibitor to control the biofilm formation of periodontopathogens
D-Galactose as an autoinducer 2 inhibitor to control the biofilm formation of periodontopathogens
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DOI：
10.1007/s12275-016-6345-8
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发表时间：
2016-09-01
影响因子：
3
通讯作者：
Choi, Bong-Kyu
中科院分区：
文献类型：
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作者：
Ryu, Eun-Ju;Sim, Jaehyun;Choi, Bong-Kyu
自体诱导物2(AI-2)是一种群体感应分子，细菌对其做出反应，调节各种表型，包括毒力和生物被膜的形成。AI-2在主要由革兰氏阴性厌氧菌组成的龈下生物膜的形成中起着重要作用，由此引发牙周炎。本研究的目的是评价D-半乳糖作为抑制AI-2活性从而抑制牙周病原体生物膜形成的作用。在寻找核梭杆菌AI-2受体的过程中，D-半乳糖结合蛋白(GBP，基因ID为FN1165)与已知的放线杆菌AI-2受体核糖结合蛋白(RbsB)具有很高的序列相似性。评价了D-半乳糖对哈维氏弧菌BB152和连接牙科生物膜中早期定植共生体和晚期致病定殖体的主要共聚合桥生物核心菌AI-2活性的抑制作用。用结晶紫染色和激光共聚焦扫描显微镜观察D-半乳糖对牙周病原菌生物膜形成的抑制作用。D-半乳糖显著抑制哈维氏弧菌和核弧菌的AI-2活性。此外，D-半乳糖对核盘藻AI-2诱导的核盘藻、牙龈卟啉单胞菌和连翘坦纳氏菌的生物膜形成有明显的抑制作用，而不影响细菌的生长。我们的结果表明，GBP可能作为AI-2受体发挥作用，半乳糖可能通过靶向AI-2活性来防止牙周病原体生物膜的形成。
Autoinducer 2 (AI-2) is a quorum sensing molecule to which bacteria respond to regulate various phenotypes, including virulence and biofilm formation. AI-2 plays an important role in the formation of a subgingival biofilm composed mostly of Gram-negative anaerobes, by which periodontitis is initiated. The aim of this study was to evaluate D-galactose as an inhibitor of AI-2 activity and thus of the biofilm formation of periodontopathogens. In a search for an AI-2 receptor of Fusobacterium nucleatum, D-galactose binding protein (Gbp, Gene ID FN1165) showed high sequence similarity with the ribose binding protein (RbsB), a known AI-2 receptor of Aggregatibacter actinomycetemcomitans. D-Galactose was evaluated for its inhibitory effect on the AI-2 activity of Vibrio harveyi BB152 and F. nucleatum, the major coaggregation bridge organism, which connects early colonizing commensals and late pathogenic colonizers in dental biofilms. The inhibitory effect of D-galactose on the biofilm formation of periodontopathogens was assessed by crystal violet staining and confocal laser scanning microscopy in the absence or presence of AI-2 and secreted molecules of F. nucleatum. D-Galactose significantly inhibited the AI-2 activity of V. harveyi and F. nucleatum. In addition, D-galactose markedly inhibited the biofilm formation of F. nucleatum, Porphyromonas gingivalis, and Tannerella forsythia induced by the AI-2 of F. nucleatum without affecting bacterial growth. Our results demonstrate that the Gbp may function as an AI-2 receptor and that galactose may be used for prevention of the biofilm formation of periodontopathogens by targeting AI-2 activity.