Sims T J, Moncla B J, Darveau R P, Page R C
Research Center in Oral Biology, University of Washington, Seattle 98195.
Infect Immun. 1991 Mar;59(3):913-24. doi: 10.1128/iai.59.3.913-924.1991.
Most juvenile periodontitis patients respond to infection by Actinobacillus actinomycetemcomitans by producing serum antibodies. Specific antigens inducing the humoral immune response have not been identified, nor has the role of the resulting antibodies in disease progression been determined. Adsorbed and unadsorbed sera from juvenile periodontitis patients and normal subjects were analyzed by enzyme-linked immunosorbent assay and Western blots (immunoblots), using digested and undigested bacterial sonicates and French pressure cell fractions to determine the biochemical class, cross-reactivity, and cellular location of the antigens in different A. actinomycetemcomitans serotypes. Antigens detected by using high-titer sera included the following: (i) serotype-specific nonprotein material located on the cell surface, (ii) soluble-fraction proteins showing highly variable antibody binding, (iii) cross-reactive proteins, and (iv) a protein present in soluble and cell wall fractions and immunopositive for all sera tested. In addition, one apparently nonprotein component that was enriched in the cell wall fraction was observed. Sera with high immunoglobulin G titers to one, two, three, or none of the three A. actinomycetemcomitans serotypes were observed. There was a high degree of variation from one patient to another in the humoral immune response to serotype-specific and cross-reactive antigens. As demonstrated by whole-cell adsorption experiments, the serotype-specific surface antigen accounted for approximately 72 to 90% of the total antibody-binding activity for sera with titers greater than 100-fold above background, while cross-reactive antigen accounted for less than 28%. Antibody binding the whole-cell sonicate for high-titer sera was inhibited 90% by lipopolysaccharide from the same serotype, strongly suggesting that lipopolysaccharide is the immunodominant antigen class.
大多数青少年牙周炎患者通过产生血清抗体来应对伴放线放线杆菌感染。尚未确定诱导体液免疫反应的特异性抗原，也未明确所产生的抗体在疾病进展中的作用。通过酶联免疫吸附测定和蛋白质印迹法（免疫印迹法），使用经消化和未经消化的细菌超声裂解物以及法国压榨细胞组分，对青少年牙周炎患者和正常受试者的吸附血清和未吸附血清进行分析，以确定不同伴放线放线杆菌血清型中抗原的生化类别、交叉反应性和细胞定位。使用高效价血清检测到的抗原包括：（i）位于细胞表面的血清型特异性非蛋白质物质，（ii）显示出高度可变抗体结合的可溶性组分蛋白，（iii）交叉反应性蛋白，以及（iv）一种存在于可溶性组分和细胞壁组分中且对所有测试血清呈免疫阳性的蛋白。此外，还观察到一种在细胞壁组分中富集的明显非蛋白质成分。观察到对三种伴放线放线杆菌血清型中的一种、两种、三种或无血清型具有高免疫球蛋白G效价的血清。在对血清型特异性和交叉反应性抗原的体液免疫反应方面，患者之间存在高度差异。如全细胞吸附实验所示，血清型特异性表面抗原占效价比背景高100倍以上的血清总抗体结合活性的约72%至90%，而交叉反应性抗原占比不到28%。来自相同血清型的脂多糖可抑制高效价血清与全细胞超声裂解物的抗体结合达90%，强烈表明脂多糖是免疫显性抗原类别。
