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

我们之前报道过在牙龈卟啉单胞菌ATCC 33277细胞表面表达两种不同类型的菌毛。大多数传染病的初始事件包括病原体粘附到宿主组织和随后病原体的入侵。为了确定毛在牙龈卟啉单胞菌粘附和侵袭上皮细胞中的作用，我们构建了毛突变体。观察牙龈假单胞菌菌毛在大鼠牙槽骨吸收过程中的作用。通过同源重组技术获得41-K纤维蛋白基因（fimA）和/或67-K纤维蛋白基因（mfa1）失活突变体，并比较fimA突变体（MPG1）、mfa1突变体（MPG67）和双敲除突变体（MPG4167）。在人口腔上皮KB细胞中评估牙龈假单胞菌的粘附性和侵袭性。我们用一个大鼠模型来检验每种类型的菌毛在口腔感染引起的牙槽骨丢失中的作用。突变体的粘附和侵袭水平均低于野生型菌株。MPG1感染的大鼠骨质流失明显高于MPG67感染的大鼠。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质流失明显减少。本研究数据提示，除了41-K毛缘蛋白外，67-K毛缘蛋白在牙周病的发病过程中也起着重要作用。

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.