HOST-BACTERIAL INTERACTIONS IN PERIODONTAL DISEASE

牙周炎是一种慢性牙周组织炎症性疾病 以疾病活动的爆发和更长时间的 缓解。 结扎引起的牙周炎提供了一个类似的模型， 微生物菌群，其中疾病的速度可以加快。 先前 研究表明，用热杀死类杆菌的免疫 在结扎引起的牙周炎中，Macalloy提供了一些保护作用 模型通过减少B.严重程度和 与假免疫，结扎和免疫， 未连接的对照。 这一建议扩展了先前的意见， 试图增强“保护性”体液反应，并评估 细菌因素负责改变其发病机制 结扎引起的牙周炎。 具体目标是：1.隔离 来自B的荚膜和膜部分。真可怕。 2.识别 最有可能引起保护性反应的组分。 猴血清 可从以前的赠款支持的研究和兔抗血清， 将制备级分，并通过体外测定来评价它们的 对定植和传染性的潜在影响。 这些将包括 抗血清对组分调理作用、共聚集 与其他口腔细菌，并坚持上皮细胞。 3.审查 用所选细菌级分免疫对 结扎引起的猴子牙周炎。 这将被描述为 临床、组织学、微生物学和免疫学基础。 4.评估免疫如何在结扎过程中提供保护。 因素 要考虑的因素包括细菌、血清 细菌的调理作用，细菌共聚集，和细菌 粘附于上皮。 这一建议将提供一个更好的理解的发病机制， 牙周炎，并将潜在的治疗价值。

Human periodontitis is a chronic inflammatory disease of the periodontium characterized by bursts of disease activity and longer periods of remission. Ligature-induced periodontitis provides a model with a similar microflora in which the rate of disease can be accelerated. Previous studies have demonstrated that immunization with heat killed Bacteroides macacae provides some protection in the ligature induced periodontitis model by reducing both the recolonization by B. macacae and the extent of alveolar bone loss compared to the sham-immunized, ligated and immunized, mon-ligated controls. This proposal extends these earlier observations and attempts to enhance the "protective" humoral response and evaluate which bacterial factors are responsible for modifying the pathogenesis of ligature induced periodontitis. The specific aims are to: 1. Isolate capsular and membrane fractions from B. macacae. 2. Identify the fraction(s) most likely to evoke a protective response. Monkey sera available from the previous grant supported studies and rabbit antisera to the fractions will be prepared ad evaluated by in vitro assays for their potential influence on colonization and infectivity. These will include the effects of antisera to the fractions on opsonization, coaggregation with other oral bacteria, and adherence to epithelial cells. 3. Examine the effects of immunization with the selected bacterial fraction on ligature-induced periodontitis in monkeys. This will be characterized on the basis of clinical, histological, microbiological and immunological. 4. Evaluate how immunization confers protection during ligation. Factors to be considered include tissue invasion by the bacteria, serum opsonization of the bacteria, bacterial co-aggregation, and bacterial adherence to epithelium. This proposal would provide a better understanding of the pathogenesis of periodontitis and would potentially be of value in treatment.