HUMAN ANTIBODY RESPONSIVENESS AND DENTAL CARIES

首席研究员在人体上的研究表明， 血清中口腔细菌抗体的沉淀与 龋病严重程度和牙周积累量有显著差异 细菌菌斑。一种抗体与发现的表位一起沉淀 放线菌属中的大分子另一种是D-丙氨酸乙酯 链球菌和乳杆菌中甘油磷壁酸的含量。 非沉淀性血清多聚磷酸甘油抗体 后一种抗原与龋病严重程度无关。D-丙氨基 酯表位在pH为5时稳定，但在生理pH下迅速降解。 本研究的主要具体目的是定量测定血清和 灵敏的酶免疫分析法检测唾液抗体对各表位的反应 为了研究表位特异性局部和表位之间的关系 全身抗体反应、年龄、龋齿严重程度和斑块堆积。 第二个目的是阐明基因构成在反应中的作用。 发展。血清免疫球蛋白和分泌型免疫球蛋白A来源于不同的发病模式 抗原暴露，分别表示全身或局部免疫 回应。培养滤液或细胞提取液中的相应抗原 变形链球菌GS-4和粘性葡萄球菌ATCC 19246，将被涂在 微孔板与血清或唾液样本抗体含量的关系 下定决心。在没有或存在抗体的情况下结合的抗体量 适当的半抗原将与碱性磷酸酶共价测定 人免疫球蛋白或分泌链与山羊免疫球蛋白的偶联 人类免疫球蛋白A。抑制前后结合的差异将 反映表位特异性抗体结合，并将通过 与适当的、反应强烈的血清进行比较。两国关系 与沉淀素反应结合的表位特异性抗体的内容 将通过多重判别分析进行检验。相互关系 各自的抗体含量，年龄，龋齿严重程度， 接触氟的时间长短、菌斑堆积和牙周炎 通过对整个人群的多元回归分析和 在不同的血清和唾液抗体反应组内。差异在于 龋病严重程度与人类白细胞抗原A、B、C、DR特异性表达的关系 分别由抗体反应组进行多项检查 判别分析。这一发现应该会确定与此相关的新因素 具有防龋性和易感性。

Studies in humans by the principal investigator have shown that precipitating serum antibodies to oral bacteria are associated with significant differences in dental caries severity and accumulation of bacterial plaque. One antibody precipitates with an epitope found on macromolecules from Actinomyces spp. and the other with the D-alanyl ester moeity of glycerol teichoic acids from Streptococci and Lactobacilli. Non-precipitating serum antibodies to the polyglycerol phosphate moeity of the latter antigen are not associated with caries severity. The D-alanyl ester epitope is stable at pH 5, but hydrolyses rapidly at physiologic pH. The major specific aim of this study is to quantitate the serum and salivary antibody response to each epitope by a sensitive enzymoimmunoassay in order to examine the relationships between epitope-specific local and systemic antibody responses, age, caries severity and plaque accumulation. A secondary aim is to elucidate a role for genetic constitution in response development. Serum IgG and secretory IgA originate from different modes of antigen exposure and respectively indicate systemic or local immune responses. The respective antigens, in culture filtrates or cell extracts of S. mutans GS-4 and A. viscosus ATCC 19246, will be coated on wells of microplates and the antibody content of serum or salivary samples determined. The amount of antibody bound in the absence or presence of appropriate haptens will be measured with alkaline phosphatase covalently conjugated to goat IgG specific for either human IgG or the secretory chain of human IgA. The difference in binding before and after inhibition will reflect epitope-specific antibody binding and will be quantified by comparison with an appropriate, strongly reactive serum. The relationship of the epitope-specific antibody binding contents to precipitin responses will be examined by multiple discriminant analysis. The interrelationship of the respective antibody contents to each other, age, caries severity, length of fluoride exposure, plaque accumulation and gingivitis will be examined by multiple regression analysis over the whole population and within various serum and saliva antibody response groups. Differences in caries severity or expression of HLA-A, B, C and DR specificities respectively by antibody response group will be examined by multiple discriminant analysis. The findings should identify new factors associated with caries protection and susceptibility.