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首页> 外文期刊>Journal of bacteriology >Inactivation of the Porphyromonas gingivalis fimA gene blocks periodontal damage in gnotobiotic rats.
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Inactivation of the Porphyromonas gingivalis fimA gene blocks periodontal damage in gnotobiotic rats.

机译：牙龈卟啉单胞菌fimA基因的失活阻断了致癌大鼠的牙周损伤。

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摘要

Fimbrial production by Porphyromonas gingivalis was inactivated by insertion-duplication mutagenesis, using the cloned gene for the P. gingivalis major fimbrial subunit protein, fimA. by several criteria, this insertion mutation rendered P. gingivalis unable to produce fimbrilin or an intact fimbrial structure. A nonfimbriated mutant, DPG3, hemagglutinated sheep erythrocytes normally and was unimpaired in the ability to coaggregate with Streptococcus gordonii G9B. The cell surface hydrophobicity of DPG3 was also unaffected by the loss of fimbriae. However, DPG3 was significantly less able to bind to saliva-coated hydroxyapatite than wild-type P. gingivalis 381. This suggested that P. gingivalis fimbriae are important for adherence of the organism to saliva-coated oral surfaces. Further, DPG3 was significantly less able to cause periodontal bone loss in a gnotobiotic rat model of periodontal disease. These observations are consistent with other data suggesting that P. gingivalis fimbriae play an important role in the pathogenesis of human periodontal disease.
机译：牙龈卟啉单胞菌的纤维产生通过插入-复制诱变而失活，使用了牙龈卟啉单胞菌主要纤维亚基蛋白fimA的克隆基因。从几个标准来看，这种插入突变使牙龈卟啉单胞菌不能产生纤维蛋白或完整的纤维结构。非成纤维的突变体DPG3正常地凝集了绵羊红细胞，并且与戈登链球菌G9B共聚集的能力没有受到损害。 DPG3的细胞表面疏水性也不受菌毛损失的影响。然而，与野生型牙龈卟啉单胞菌381相比，DPG3与唾液包覆的羟基磷灰石的结合能力显着降低。这表明牙龈卟啉单胞菌菌毛对于有机体对唾液包覆的口腔表面的粘附至关重要。此外，在牙周疾病的致病大鼠模型中，DPG3引起牙周骨丢失的能力明显降低。这些观察结果与其他数据一致，表明齿龈假单胞菌菌毛在人类牙周疾病的发病机理中起重要作用。

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