D-Galactose as an autoinducer 2 inhibitor to control the biofilm formation of periodontopathogens
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- 作者：Eun-Ju Ryu ; Jaehyun Sim ; Jun Sim ; Julian Lee ; Bong-Kyu Choi
- 关键词：quorum sensing ; periodontopathogens ; biofilm ; AI ; 2 inhibitor ; D ; galactose
- 刊名：Journal of Microbiology
- 出版年：2016
- 出版时间：September 2016
- 年：2016
- 卷：54
- 期：9
- 页码：632-637
- 全文大小：729 KB
- 刊物主题：Microbiology;
- 出版者：Springer Netherlands
- ISSN：1976-3794
- 卷排序：54
文摘
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.