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首页> 外文期刊>Infection and immunity >Kgp and RgpB, but Not RgpA, Are Important for Porphyromonas gingivalis Virulence in the Murine Periodontitis Model
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Kgp and RgpB, but Not RgpA, Are Important for Porphyromonas gingivalis Virulence in the Murine Periodontitis Model

机译:Kgp和RgpB,而不是RgpA,对于鼠牙周炎模型中的牙龈卟啉单胞菌毒力很重要

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The contributions of three proteinase genes (rgpA, rgpB, and kgp) to the virulence of Porphyromonas gingivalis W50 were investigated in the murine periodontitis model. Mice were orally inoculated with eight doses (1 × 1010 cells per dose) of rgpA, rgpB, kgp, rgpA rgpB, or rgpA rgpB kgp isogenic mutants, and the level of alveolar bone loss, immune response induced, and number of bacterial cells per half maxilla were compared with those of animals inoculated with wild-type P. gingivalis. The kgp, rgpB, rgpA rgpB, and rgpA rgpB kgp isogenic mutants induced significantly (P < 0.05) less bone loss than the rgpA isogenic mutant and the wild type did, and the virulence of the rgpA isogenic mutant and the wild type were not significantly different. Mice inoculated with the wild type or the rgpA isogenic mutant exhibited significantly (P < 0.01) more P. gingivalis cells per half maxilla than mice inoculated with rgpB, kgp, rgpA rgpB, and rgpA rgpB kgp isogenic mutants or nonchallenged mice did, as determined using real-time PCR. A significant positive correlation was found between the number of P. gingivalis cells detected per half maxilla and the amount of alveolar bone loss induced. Enzyme-linked immunosorbent assay results showed that each isogenic mutant and the wild type induced a predominant P. gingivalis antigen-specific immunoglobulin G3 (IgG3) response. Furthermore, the kgp and rgpA rgpB kgp isogenic mutants induced significantly (P < 0.05) lower IgG3 antibody responses than the responses induced by the wild type or the rgpA, rgpB, and rgpA rgpB isogenic mutants. The results suggest that the order in which the proteinases contribute to the virulence of P. gingivalis in the murine periodontitis model is Kgp ≥ RgpB >? RgpA.
机译: rgpA rgpB kgp 三种蛋白酶基因对牙龈卟啉单胞菌W50毒力的贡献在鼠牙周炎模型中进行了研究。小鼠经口接种八剂 rgpA rgpB kgp (每剂1×10 10 细胞) , rgpA rgpB rgpA rgpB kgp 等位基因突变体,比较了肺泡骨丢失的水平,诱导的免疫应答和每半个上颌的细菌细胞数量。用野生型 P接种的动物。牙龈炎 kgp rgpB rgpA rgpB rgpA rgpB kgp 等位基因突变体均引起显着诱导( P < / em> <0.05)的骨质损失少于 rgpA 同基因突变体和野生型,并且 rgpA 同基因突变体和野生型的毒力没有显着差异。用野生型或 rgpA 等基因突变体接种的小鼠表现出显着( P <0.01)更多的 P。上 rgpB kgp rgpA rgpB rgpA rgpB kgp接种的小鼠的上颌半个牙龈细胞em>等基因突变体或非挑战性小鼠的确如此,这是通过实时PCR测定的。发现 P的数量之间存在显着的正相关。每半个上颌骨检测到牙龈细胞,并引起牙槽骨丢失。酶联免疫吸附试验结果表明,每个同基因突变体和野生型均诱导了主要的 P。牙龈抗原特异性免疫球蛋白G3(IgG3)反应。此外, kgp rgpA rgpB kgp 等位基因突变体诱导的IgG3抗体反应明显低于野生型诱导的( P <0.05)或 rgpA rgpB rgpA rgpB 等基因突变体。结果表明蛋白酶对 P的毒性贡献的顺序。鼠牙周炎模型中的牙龈炎为Kgp≥RgpB >? RgpA。

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