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首页> 外文期刊>Infection and immunity >Identification of a Second Arcanobacterium pyogenes Neuraminidase and Involvement of Neuraminidase Activity in Host Cell Adhesion
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Identification of a Second Arcanobacterium pyogenes Neuraminidase and Involvement of Neuraminidase Activity in Host Cell Adhesion

机译：化脓性第二产弧菌的神经氨酸酶的鉴定和神经氨酸酶活性参与宿主细胞粘附。

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Arcanobacterium pyogenes, a common inhabitant of the upper respiratory and urogenital tracts of economically important animals, such as cattle and swine, is also an opportunistic pathogen associated with suppurative infections in these animals. A. pyogenes expresses neuraminidase activity encoded by the nanH gene, and previously, construction of a nanH mutant of A. pyogenes BBR1 indicated that a second neuraminidase is present in this strain. A 5,112-bp gene, nanP, was cloned and sequenced, and this gene conferred neuraminidase activity on an Escherichia coli host strain. The predicted 186.8-kDa NanP protein exhibited similarity to a number of bacterial neuraminidases and contained the RIP/RLP motif and five copies of the Asp box motif found in all bacterial neuraminidases. As expected, insertional inactivation of the nanP gene in A. pyogenes BBR1 resulted in a mutant with reduced neuraminidase activity. However, insertional inactivation of the nanP gene in the nanH mutant strain resulted in a complete lack of neuraminidase activity. Like NanH, NanP was localized to the A. pyogenes cell wall. However, unlike the nanH gene, which was present in 100% of the strains examined, nanP was present in only 64.2% of the isolates (n = 53). A. pyogenes adheres to HeLa cells, and a nanP mutant displayed a wild-type adhesion phenotype with these cells. In contrast, the ability of a nanH nanP double mutant to bind to HeLa cells was reduced by 53%. The wild-type adhesion phenotype was restored by providing nanP in trans. These data indicate that the neuraminidases of A. pyogenes play a role in adhesion of this organism to host epithelial cells.
机译：化脓性产气杆菌是经济上重要的动物（如牛和猪）的上呼吸道和泌尿生殖道的常见居民，也是与这些动物化脓性感染相关的机会病原体。 A。化脓的表达由 nanH 基因编码的神经氨酸酶活性，并且以前可以构建 A的 nanH 突变体。化脓性 BBR1表明该菌株中存在第二种神经氨酸酶。克隆并测序了一个5,112 bp的基因 nanP ，该基因赋予了大肠杆菌宿主菌株神经氨酸酶活性。预测的186.8 kDa NanP蛋白与许多细菌神经氨酸酶表现出相似性，并包含RIP / RLP基序和在所有细菌神经氨酸酶中​​发现的5个拷贝的Asp盒基序。如预期的那样， A中的 nanP 基因的插入失活。化脓性 BBR1导致突变的神经氨酸酶活性降低。但是， nanH 突变株中 nanP 基因的插入失活导致神经氨酸酶活性完全缺乏。像NanH一样，NanP本地化为 A。化脓细胞细胞壁。但是，与 nanH 基因不同， nanH 基因存在于100％的检测菌株中，而 nanP 仅存在于64.2％的分离株中（ n > = 53）。 A。化脓菌粘附于HeLa细胞，而 nanP 突变体表现出与这些细胞的野生型粘附表型。相反， nanH nanP 双重突变体与HeLa细胞结合的能力降低了53％。通过在 trans 中提供 nanP 来恢复野生型粘附表型。这些数据表明 A的神经氨酸酶。化脓菌在该生物与宿主上皮细胞的粘附中发挥作用。

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