A study of mechanism of adherence to the oral cavity in periodontopathic bacteria by animal model.

我们以前报道过牙龈卟啉单胞菌ATCC 33277细胞表面表达两种不同的菌毛。大多数感染性疾病的初始事件涉及病原体与宿主组织的粘附和随后的病原体入侵。为了确定菌毛在牙龈卟啉单胞菌粘附和侵袭上皮细胞中的作用，我们构建了菌毛突变体。观察牙龈卟啉单胞菌菌毛在大鼠牙槽骨侵袭和骨吸收过程中的作用。通过同源重组技术获得41-K菌毛蛋白基因（fimA）和/或67-K菌毛蛋白基因（mfa 1）的失活突变体，并在fimA突变体（MPG 1）、mfa 1突变体（MPG 67）和双敲除突变体（MPG 4167）之间进行比较。在人口腔上皮KB细胞中评估牙龈卟啉单胞菌的粘附和侵袭。我们使用大鼠模型来研究口腔感染引起的牙槽骨丢失中每种菌毛的作用。突变株的粘附和侵袭水平均低于野生型菌株。感染MPG 1的大鼠骨丢失率高于感染MPG 67的大鼠。此外，与感染野生型菌株的大鼠相比，感染双敲除突变体的大鼠的骨丢失显著降低。提示41-K菌毛蛋白和67-K菌毛蛋白在牙周病的发病机制中起重要作用。

We previously reported that the presence of two different kinds of fimbriae expressed on the cell surface of Porphyromonas gingivalis ATCC 33277. The initial event in most infectious diseases involves adhesion of pathogens to host tissues and subsequent invasion by the pathogens. To define the role of fimbriae in Porphyromonas gingivalis adherence to and invasion of epithelial cells, we have constructed fimbrial mutants. The involvement of P.gingivalis fimbriae in the invasion process and alveolar bone resorption in rats were examined. Inactivated mutants of 41-K fimbrillin gene (fimA) and/or the 67-K fimbrillin gene (mfa1) by a homologous recombination technique and compared among fimA mutant (MPG1), mfa1 mutant (MPG67), and double knockout mutant (MPG4167). Adherence and invasion of P.gingivalis was assessed in human oral epithelial KB cells. We used a rat model to examine the role of each type of fimbriae in alveolar bone loss by oral infection. The adherence and invasion levels of the mutants were lower than the wild-type strain. The bone loss of rats infected with the MPG1 was higher than that of those infected with MPG67. Moreover, the bone loss of rats infected with the double knockout mutant was significantly decreased compared to that of rats infected with the wild-type strain. Data from this study suggest that not only the 41-K fimbrial protein, but also the 67-K fimbrial protein play important roles in the pathogenesis of periodontal disease.