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HOST-BACTERIAL INTERACTIONS IN PERIODONTAL DISEASE

牙周疾病中宿主细菌的相互作用

基本信息

批准号：
3220834
负责人：
RUSSELL J NISENGARD
金额：
$ 16.64万
依托单位：
STATE UNIVERSITY OF NEW YORK AT BUFFALO
依托单位国家：
美国
项目类别：
财政年份：
1986
资助国家：
美国
起止时间：
1986-04-01 至 1994-03-31
项目状态：
已结题

项目摘要

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.

人类牙周炎是一种牙周组织的慢性炎症性疾病其特点是疾病活动爆发且持续时间较长缓解。结扎诱导的牙周炎提供了一个具有类似作用的模型可以加速疾病发生率的微生物区系。以前的研究表明，热杀死拟杆菌的免疫接种猕猴在结扎引起的牙周炎中提供一些保护模型通过减少猕猴的再定植和范围与假免疫、结扎和免疫相比，牙槽骨损失，单连接控制。该提案扩展了这些早期的观察结果并尝试增强“保护性”体液反应并评估哪些细菌因素负责改变发病机制结扎引起的牙周炎。具体目标是： 1. 隔离来自猕猴的荚膜和膜部分。 2. 识别最有可能引起保护性反应的分数。猴血清可从之前的资助研究和兔抗血清中获得将制备级分并通过体外测定对其进行评估对定植和传染性的潜在影响。这些将包括抗血清对各组分的调理作用、共聚作用的影响与其他口腔细菌，并粘附于上皮细胞。 3. 检查使用选定的细菌组分进行免疫接种的效果猴子结扎引起的牙周炎。这将被表征为临床、组织学、微生物学和免疫学基础。 4. 评估免疫接种如何在结扎过程中提供保护。因素要考虑的因素包括细菌、血清的组织侵袭细菌的调理作用、细菌共聚集和细菌与上皮细胞的粘附。该建议将有助于更好地了解该病的发病机制牙周炎，可能具有治疗价值。