SIALIDASE-ENHANCED LECTIN-LIKE MECHANISM FOR ACTINOMYCES-VISCOSUS AND ACTINOMYCES-NAESLUNDII HEMAGGLUTINATION
SIALIDASE-ENHANCED LECTIN-LIKE MECHANISM FOR ACTINOMYCES-VISCOSUS AND ACTINOMYCES-NAESLUNDII HEMAGGLUTINATION
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DOI：
10.1128/iai.27.2.335-343.1980
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发表时间：
1980-01-01
影响因子：
3.1
通讯作者：
GROVE, DA
中科院分区：
文献类型：
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作者：
ELLEN, RP;FILLERY, ED;GROVE, DA
通过标准絮凝载玻片试验研究了代表 6 个数值分类簇的实验室菌株以及人粘性放线菌和内氏放线菌的新鲜分离株对来自不同动物物种的红细胞 (RBC) 进行血凝的能力。人类AB和马RBC比其他人更频繁、更快速地凝集；豚鼠红细胞仅被少数菌株凝集。选择人类 AB 红细胞来研究血凝 [HA] 机制。用梭菌神经氨酸酶 (NTRBC) 处理红细胞可大大增强几乎所有菌株的 HA。在使用不同浓度的糖的半抗原抑制实验中，β-半乳糖苷是RBC和NTRBC的HA最有效的抑制剂；抑制 NTRBC 凝集需要更高的浓度。大豆凝集素凝集 RBC 和 NTRBC，但不凝集放线菌细胞。 NTRBC 的凝集浓度低 125 倍。对于 1 种测试菌株，HA 对 EDT 敏感。通过添加β-半乳糖苷，HA反应是可逆的。通过回收放线菌凝集的红细胞来研究放线菌菌株通过去除唾液酸以暴露更多的倒数第二个β-半乳糖苷位点来引发红细胞HA的能力，所述红细胞用乳糖溶液分散并洗去细菌（引发的RBC）。以这种方式引发通过指示放线菌菌株增强了随后的HA，并使红细胞对大豆凝集素的凝集更加敏感。放线菌菌株的引发能力通常与从引发的红细胞中去除的唾液酸量相关。代表数字分类簇的菌株在 HA 和启动活性方面有所不同。簇 5 菌株（典型的 A. naeslundii）是 RBC、NTRBC 和引发的 RBC 的良好凝集剂，但引物较差。簇 3 菌株（非典型内氏放线菌）是最弱的 HA 诱导剂，但可以充分启动红细胞，以供其他菌株随后进行凝集。放线菌HA可通过两步机制进行：神经氨酸酶去除末端唾液酸和凝集素样结合至RBC上暴露的β-半乳糖苷相关位点。菌株在执行这两种功能的程度上有所不同，这种特异性可能与其分类学分类有关。放线菌在牙周病变发病机制中的作用探讨
Laboratory strains representing 6 numerical taxonomy clusters and fresh isolates of human A. viscosus and A. naeslundii were studied by standard flocculation slide tests for the ability to hemagglutinate erythrocytes (RBC) from various animal species. Human AB and horse RBC were agglutinated more frequently and rapidly than others; guinea pig RBC were agglutinated by only a few strains. Human AB RBC were selected for studies of hemagglutination [HA] mechanisms. Treatment of RBC with clostridial neuraminidase (NTRBC) greatly enhanced HA for almost all strains. In hapten inhibition experiments in which various concentrations of sugars were used, .beta.-galactosides were the most effective inhibitors of HA for RBC and NTRBC; inhibition of NTRBC agglutination required higher concentrations. Soybean lectin agglutinated RBC and NTRBC but not Actinomyces cells. NTRBC agglutinated at a 125-fold-lower concentration. HA was sensitive to EDT for 1 strain tested. HA reactions were reversible by addition of .beta.-galactosides. The ability of Actinomyces strains to prime RBC for HA by removing sialic acid to expose more penultimate .beta.-galactoside sites was studied by recycling Actinomyces-agglutinated RBC which were dispersed with a lactose solution and washed free of bacteria (primed RBC). Priming in this manner augmented subsequent HA by indicator Actinomyces strains and made the RBC more sensitive to agglutination by soybean lectin. The priming ability of Actinomyces strains generally correlated with the amount of sialic acid removed from primed RBC. Strains representing the numerical taxonomy clusters differed in their HA and priming activities. Cluster 5 strains (typical A. naeslundii) were good agglutinators of RBC, NTRBC and primed RBC but were poor primers. Cluster 3 strains (atypical A. naeslundii) were the weakest HA inducers but could prime RBC adequately for subsequent agglutination by other strains. Actinomyces HA may proceed via a 2-step mechanism: neuraminidase removal of terminal sialic acid and lectin-like binding to exposed .beta.-galactoside-associated sites on the RBC. Strains differ in the extent to which they can perform the 2 functions and this specificity may relate to their taxonomic classification. [The role of Actinomyces in the pathogenesis of periodontal lesions is discussed].