Abiotrophia defectiva is a species of nutritionally variant streptococci that is found in human saliva and dental plaques and that has been associated with infective endocarditis. In our previous study, it was found that A. defectiva could bind specifically to saliva‐coated hydroxyapatite beads (SHA). This study identified a cell surface component of A. defectiva that promotes adherence to SHA beads. The binding of A. defectiva to SHA was reduced in the presence of antibodies against human proline‐rich protein (PRP); these results suggested that PRP may be a critical component mediating interactions between A. defectiva and the salivary pellicle. Two‐dimensional gel electrophoresis of whole A. defectiva cells followed by Far‐Western blotting was conducted by probing with synthetic peptides analogous to the binding region of PRP known as PRP‐C. The results indicate that an A. defectiva protein of 37 kDa interacts with PRP‐C. The results of amino‐terminal sequencing of the adhesive A. defectiva protein revealed significant similarity to glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH). Recombinant GAPDH bound to immobilized PRP‐C in a dose‐dependent manner and binding of A. defectiva to SHA or to PRP was reduced in the presence of anti‐GAPDH antiserum. Western blotting or electron immunomicroscopic observations with anti‐GAPDH antiserum revealed that this protein was expressed in both cytosolic and cell wall fractions. These results suggest that A. defectiva could specifically bind to PRP via interactions with cell surface GAPDH; the findings suggest a mechanism underlying A. defectiva‐mediated adherence to saliva‐coated tooth surfaces.

中文翻译：

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缺水营养菌通过唾液富含脯氨酸的蛋白质与细菌甘油醛-3-磷酸脱氢酶之间的相互作用，粘附在唾液包覆的羟基磷灰石珠上。

缺营养厌食菌是一种营养变异链球菌，存在于人的唾液和牙菌斑中，并与感染性心内膜炎有关。在我们之前的研究中，发现缺陷果曲霉可以与唾液包被的羟基磷灰石珠（SHA）特异性结合。这项研究确定了缺陷果曲霉的细胞表面成分，该成分促进了对SHA珠的粘附。在抗人脯氨酸丰富蛋白（PRP）抗体存在下，缺陷曲霉与SHA的结合减少；这些结果表明，PRP可能是介导曲霉和唾液薄膜之间相互作用的关键成分。整个缺陷曲霉的二维凝胶电泳通过用类似于PRP结合区（称为PRP-C）的合成肽探测细胞，然后进行Far-Western印迹。结果表明，一个A. defectiva用PRP-C的37个kDa的相互作用蛋白。黏附缺陷曲霉蛋白的氨基末端测序结果表明，其与甘油醛-3-磷酸脱氢酶（GAPDH）极为相似。重组GAPDH以剂量依赖的方式与固定的PRP-C结合，在存在抗GAPDH抗血清的情况下，缺陷曲霉与SHA或PRP的结合减少。用抗GAPDH抗血清进行的蛋白质印迹或电子免疫显微镜观察表明，该蛋白在细胞溶质和细胞壁组分中均表达。这些结果表明缺陷假单胞菌可以通过与细胞表面GAPDH的相互作用特异性结合PRP。这些发现提示了一种由A.缺损介导的对唾液覆盖的牙齿表面粘附的机制。