Department of Oral Microbiology and Immunology, School of Dentistry, Seoul National University, Seoul, Republic of Korea.
Arch Oral Biol. 2013 Jan;58(1):17-27. doi: 10.1016/j.archoralbio.2012.04.016. Epub 2012 May 26.
Periodontitis is initiated by bacteria in subgingival biofilms, which are composed mostly of Gram-negative anaerobes. Autoinducer 2 (AI-2) is a universal quorum sensing (QS) molecule that mediates intergeneric signalling in multispecies bacterial communities and may induce biofilm formation. As Fusobacterium nucleatum is the major coaggregation bridge organism that links early colonising commensals and late pathogenic colonisers in dental biofilms via the accretion of periodontopathogens, we hypothesised that AI-2 of F. nucleatum contributes to this interspecies interaction, and interruption of this signalling could result in the inhibition of biofilm formation of periodontopathogens. To test this hypothesis, we evaluated the effect of partially purified F. nucleatum AI-2 on monospecies biofilm as well as mutualistic interactions between F. nucleatum and the so-called 'red complex' (Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia). Then we tested the effect of two QS inhibitors (QSIs), (5Z)-4-bromo-5-(bromomethylene)-2(5H)-furanone (furanone compound) and d-ribose, on AI-2-induced biofilm formation and coaggregation. F. nucleatum AI-2 remarkably induced biofilm growth of single and dual species and coaggregation between F. nucleatum and each species of the 'red complex', all of which were inhibited by the QSIs. F. nucleatum AI-2 induced the expression of the representative adhesion molecules of the periodontopathogens, which were inhibited by the QSIs. Our results demonstrate that F. nucleatum AI-2 plays an important role in inter- and intraspecies interactions between periodontopathogens via enhanced expression of adhesion molecules and may be a target for the inhibition of pathogenic dental biofilm formation.
牙周炎是由龈下生物膜中的细菌引发的，生物膜主要由革兰氏阴性厌氧菌组成。自体诱导物 2（AI-2）是一种普遍的群体感应（QS）分子，可介导多物种细菌群落中的种间信号传递，并可能诱导生物膜形成。由于核梭杆菌是主要的共聚集桥接生物体，通过牙周病原体的积累，将早期定植的共生菌与晚期定植的病原菌连接在牙生物膜中，我们假设核梭杆菌的 AI-2 有助于这种种间相互作用，并且这种信号的中断可能导致牙周病原体生物膜形成的抑制。为了验证这一假设，我们评估了部分纯化的核梭杆菌 AI-2 对单物种生物膜以及核梭杆菌与所谓的“红色复合物”（牙龈卟啉单胞菌、齿密螺旋体和福赛坦纳氏菌）之间的共生相互作用的影响。然后，我们测试了两种 QS 抑制剂（QSIs）（5Z）-4-溴-5-（溴亚甲基）-2（5H）-呋喃酮（呋喃酮化合物）和 D-核糖对 AI-2 诱导的生物膜形成和共聚集的影响。核梭杆菌 AI-2 显著诱导了单种和双种生物膜的生长以及核梭杆菌与“红色复合物”中每种物种的共聚集，所有这些都被 QSIs 抑制。核梭杆菌 AI-2 诱导了牙周病原体代表性粘附分子的表达，这些表达被 QSIs 抑制。我们的结果表明，核梭杆菌 AI-2 通过增强粘附分子的表达在牙周病原体的种间和种内相互作用中发挥重要作用，并且可能是抑制致病牙生物膜形成的靶标。
