Vasel D, Sims T J, Bainbridge B, Houston L, Darveau R, Page R C
Regional Clinical Dental Research Center, School of Medicine, University of Washington, USA.
Oral Microbiol Immunol. 1996 Aug;11(4):226-35. doi: 10.1111/j.1399-302x.1996.tb00174.x.
Periodontitis in humans is caused by a group of predominantly gram-negative, anaerobic bacteria among which Porphyromonas gingivalis and Bacteroides forsythus are prominent. A similar group is present and presumably plays a similar role in experimental periodontitis in the primate Macaca fascicularis. Nevertheless, immunization using a vaccine containing only killed P. gingivalis suppresses the progress of experimental periodontitis in M. fascicularis. We investigated the hypothesis that gram-negative periodontopathic bacterial may share antigens, and immunization with one species may induce antibodies reactive with other gram-negative species. Using enzyme-linked immunosorbent assay (ELISA), Western and dot immunoblots with nonabsorbed and absorbed and immune and preimmune sera we show that monkeys immunized with P. gingivalis produce antibodies reactive not only with antigens of P. gingivalis but also with those of B. forsythus. Similarly, rabbits immunized with P. gingivalis or with B. forsythus produce antibodies that react with antigens of both bacteria. Cross-reactive antibodies bind to epitopes in lipid A and possibly in core carbohydrate of lipopolysaccharide. Using complexes of lipopolysaccharide with polymyxin B, bovine serum albumin and apolipoprotein A1 specificity of binding was documented. Using sera from monkeys immunized with P. gingivalis, cross-reactivity with Actinobacillus actinomycetemcomitans could not be demonstrated by ELI-SA, although binding to lipopolysaccharide but not to lipid A was demonstrated by Western and dot immunoblots. Antibodies to shared lipopolysaccharide epitopes of periodontopathic bacteria may account, at least in part, for the immune protection observed in immunized monkeys, and shared epitopes may have potential as a vaccine for periodontitis in humans.
人类牙周炎是由一组主要为革兰氏阴性厌氧菌引起的，其中牙龈卟啉单胞菌和福赛坦氏菌较为突出。在猕猴的实验性牙周炎中也存在类似的菌群，并且可能发挥类似的作用。然而，使用仅含有灭活牙龈卟啉单胞菌的疫苗进行免疫可抑制猕猴实验性牙周炎的进展。我们研究了革兰氏阴性牙周病原菌可能共享抗原的假说，用一种菌种进行免疫可能诱导出与其他革兰氏阴性菌种发生反应的抗体。我们使用酶联免疫吸附测定（ELISA）、蛋白质免疫印迹法和斑点免疫印迹法，用未吸收和吸收的、免疫和免疫前的血清进行检测，结果表明，用牙龈卟啉单胞菌免疫的猴子产生的抗体不仅能与牙龈卟啉单胞菌的抗原发生反应，还能与福赛坦氏菌的抗原发生反应。同样，用牙龈卟啉单胞菌或福赛坦氏菌免疫的兔子产生的抗体能与两种细菌的抗原发生反应。交叉反应抗体与脂多糖的脂质A以及可能的核心碳水化合物中的表位结合。使用脂多糖与多粘菌素B、牛血清白蛋白和载脂蛋白A1的复合物证明了结合的特异性。用牙龈卟啉单胞菌免疫的猴子的血清，ELISA未显示与伴放线放线杆菌有交叉反应，尽管蛋白质免疫印迹法和斑点免疫印迹法显示能与脂多糖结合但不能与脂质A结合。针对牙周病原菌共享脂多糖表位的抗体可能至少部分解释了在免疫猴子中观察到的免疫保护作用，并且共享表位可能具有作为人类牙周炎疫苗的潜力。
