ADHERENCE OF PERIODONTAL DISEASE-ASSOCIATED BACTERIA

牙周病是成年人牙齿脱落的主要原因。 认识到微生物通过特定的生物粘附在牙齿等组织上， 结构（即，adhesins）表明，可能会制定制度， 抑制粘附和定殖。 牙周炎的发病机制 与疾病相关的微生物附着在牙齿上， 如果牙周病是以这种方式控制的话。 该项目是我们对细胞凋亡机制研究的继续。 粘性放线菌和A.内氏菌到牙齿 一个刻面 该项目的目的是表征受体结合区的 1型菌毛介导A.粘性到 唾液处理的羟基磷灰石（SHA）在体外。 这些研究报告将 方法是免疫化学分析分离的片段， 使用SDS-PAGE凝胶和蛋白质印迹分析免疫球蛋白。 通过组合 SDS-PAGE、HPLC和Western Blot技术与受体结合 抑制试验，我们计划识别和分离受体结合 区域1型菌毛介导对SHA的吸附。 一旦这个 片段已被确定为单特异性和单克隆抗体将 然后，我们将检查1型菌毛从其他 放线菌菌株，以确定是否受体结合 这些菌株的区域与菌株T14 V的区域交叉反应。 我们越 计划使用菌株T14 V的菌毛缺陷突变株来测定 如果1型和2型菌毛在粘附中的拟议作用， 体外建立的定殖可以在人体内得到证实， 小鼠 研究表明，局部免疫小鼠的牙齿， 具有这些菌毛混合物的唾液腺区域是 当受到该细菌菌株的挑战时， 扩大 这些研究将确定最佳剂量和途径， 免疫，以及1型或2型菌毛是否单独作为 有效的免疫原作为混合物。 所需的角色 菌毛特异性唾液伊加在抑制吸附或减少 还将评估殖民化。 设立的主要机构 通过用以下疫苗接种来减少菌株T14 V在小鼠牙齿中的定殖 菌毛粘附素应该有助于防止其他 牙周病原体的疫苗接种与其他菌毛粘附素。

Periodontal diseases are a major cause of tooth loss in adults. Recognition that microorganisms adhere to tissues such as teeth by specific structures (i.e., adhesins) suggest that regimes might be developed to inhibit adherence and colonization. The mechanisms by which periodontal disease-associated microorganisms attach to an accumulate on the teeth must be understood if periodontal diseases are to be controlled in this manner. The proposed project is a continuation of our studies on the mechanisms of adsorption by Actinomyces viscosus and A. naeslundii to teeth. One facet of the project is directed at characterizing the receptor binding region of the type 1 fimbriae which mediates attachment of A. viscosus to saliva-treated hydroxyapatite (SHA) in vitro. These studies will be approached be immunochemical analysis of isolated fragments of the immunoglobulins using SDS-PAGE gels and Western Blots. By combining the SDS-PAGE, HPLC, and Western Blot techniques with the receptor binding inhibition assay we plan to identify and isolate the receptor binding region type 1 fimbriae which mediates adsorption to SHA. Once this fragment has been identified monospecific and monoclonal antibodies will be prepared against it. We will then examine type 1 fimbriae from other Actinomyces strains to determine whether or not the receptor binding regions of these strains cross-react with that of strain T14V. Further we plan to use fimbrial-deficient mutant strains of strain T14V to determine if the proposed roles for type 1 and type 2 fimbriae in adherence and colonization established in vitro can be confirmed in vivo in humans and mice. Studies demonstrating that the teeth of mice immunized locally in the region of the salivary gland with a mixture of these fimbriae are resistant to colonization when challenged by that bacterial strain, will be expanded. These studies will determine the optimum dose and route of immunization, and whether type 1 or type 2 fimbriae singlely is as effective an immunogen as the mixture. The required role for fimbriae-specific salivary IgA in inhibiting adsorption or reducing colonization will also be evaluated. The principals established for reducing strain T14V colonization of teeth in mice by vaccination with fimbrial adhesins should by helpful in preventing colonization of other periodontopathogens by vaccination with other fimbrial adhesins.