Kuramitsu Howard K, Chen Wen, Ikegami Aki
Department of Oral Biology, University at Buffalo, Buffalo, NY 14214, USA.
J Periodontol. 2005 Nov;76(11 Suppl):2047-51. doi: 10.1902/jop.2005.76.11-S.2047.
Periodontitis develops as a result of the interaction of the host with subgingival plaque bacteria. Both Porphyromonas gingivalis and Treponema denticola are frequently associated together in these oral biofilms.
The molecular basis for in vitro biofilm formation was investigated for P. gingivalis 381, T. denticola 35405, and mixtures of the two organisms using microtiter plate assays. In addition, the biofilms were examined following confocal laser scanning microscopy.
P. gingivalis 381, but not T. denticola strains, formed biofilms in vitro. This property was dependent, in part, on the strain 381 fimA, ppk, and usp genes. Microarray and Northern blot analyses suggested that the expression of the ppk gene was required for maximal expression of the uspA gene. P. gingivalis 381 formed synergistic biofilms when incubated with T. denticola strains. This process was dependent upon the strain 381 rgpB and fimA genes as well as the T. denticola flgE and cfpA genes.
P. gingivalis 381 formed synergistic biofilms with T. denticola 35405. These results may be relevant to the previous observations that the two organisms are frequently observed together in subgingival plaque with the spirochetes localized to the exterior of the oral biofilms. It is suggested that other such synergistic effects may also occur between other plaque bacteria.
牙周炎是宿主与龈下菌斑细菌相互作用的结果。牙龈卟啉单胞菌和齿垢密螺旋体在这些口腔生物膜中经常共同存在。
使用微量滴定板分析法研究牙龈卟啉单胞菌381、齿垢密螺旋体35405以及这两种微生物混合物体外生物膜形成的分子基础。此外,在共聚焦激光扫描显微镜检查后对生物膜进行检测。
牙龈卟啉单胞菌381能在体外形成生物膜,而齿垢密螺旋体菌株则不能。此特性部分取决于381菌株的fimA、ppk和usp基因。微阵列和Northern印迹分析表明,ppk基因的表达是uspA基因最大表达所必需的。牙龈卟啉单胞菌381与齿垢密螺旋体菌株一起培养时会形成协同生物膜。这个过程取决于381菌株的rgpB和fimA基因以及齿垢密螺旋体的flgE和cfpA基因。
牙龈卟啉单胞菌381与齿垢密螺旋体35405形成协同生物膜。这些结果可能与之前的观察结果相关,即这两种微生物在龈下菌斑中经常共同出现,且螺旋体定位于口腔生物膜的外部。有人提出,其他菌斑细菌之间也可能发生其他此类协同作用。