ADHERENCE OF PERIODONTAL DISEASE-ASSOCIATED BACTERIA

牙周病相关细菌的粘附

• 批准号: 3219428
• 负责人: WILLIAM B CLARK
• 金额: $ 10.93万
• 依托单位: UNIVERSITY OF FLORIDA
• 依托单位国家: 美国
• 财政年份: 1979
• 资助国家: 美国
• 起止时间: 1979-04-01 至 1988-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3219428
• 关键词: Actinomyces; cell adhesion; chromatography; enzyme linked immunosorbent assay; genetic strain; gingival sulcus; human tissue; immunization; immunochemistry; immunoelectrophoresis; microorganism immunology; monoclonal antibody; mutant; oral bacteria; oral mucosa; periodontium disorder; physical chemical interaction; pilus; preventive dentistry; saliva; serum; tissue /cell culture

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.

牙周疾病是成人牙齿脱落的主要原因。 认识到微生物通过特定的方式粘附在牙齿等组织上 结构（即粘附素）表明可以开发政权 抑制粘附和定植。 牙周病的机制 与疾病相关的微生物附着在牙齿上的积聚物上 如果牙周病要以这种方式得到控制，那就可以理解了。 拟议的项目是我们对机制研究的延续 粘性放线菌和内氏放线菌对牙齿的吸附。 一个方面 该项目的目的是表征受体结合区域 1 型菌毛介导粘性 A. 粘性附着 体外唾液处理的羟基磷灰石（SHA）。 这些研究将 对分离片段进行免疫化学分析 使用 SDS-PAGE 凝胶和蛋白质印迹分析免疫球蛋白。 通过结合 SDS-PAGE、HPLC 和蛋白质印迹技术与受体结合 抑制测定我们计划识别和分离受体结合 介导 SHA 吸附的 1 型菌毛区域。 一旦这个 片段已被鉴定为单特异性，单克隆抗体将被 做好了应对准备。 然后我们将检查来自其他物种的 1 型菌毛 放线菌菌株判断受体是否结合 这些菌株的区域与菌株 T14V 的区域发生交叉反应。 进一步我们 计划使用T14V菌株的菌毛缺陷突变株来确定 如果 1 型和 2 型菌毛的拟议作用在坚持和 体外建立的定植可以在人体体内得到证实 老鼠。 研究表明，小鼠的牙齿在 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，将能够抵抗定植 扩大了。 这些研究将确定最佳剂量和途径 免疫接种，以及 1 型菌毛还是 2 型菌毛单独作为 作为混合物有效的免疫原。 所需的角色为 菌毛特异性唾液 IgA 抑制吸附或减少 殖民化也将受到评估。 设立的校长是为了 通过接种疫苗减少小鼠牙齿中 T14V 株的定植 菌毛粘附素应该有助于防止其他细菌的定植 通过接种其他菌毛粘附素来消灭牙周病原体。