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首页> 外文期刊>Infection and immunity >Insertional Inactivation of eap in Staphylococcus aureus Strain Newman Confers Reduced Staphylococcal Binding to Fibroblasts
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Insertional Inactivation of eap in Staphylococcus aureus Strain Newman Confers Reduced Staphylococcal Binding to Fibroblasts

机译：金黄色葡萄球菌菌株纽曼的插入插入失活减少了葡萄球菌与成纤维细胞的结合。

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To initiate invasive infection, Staphylococcus aureus must adhere to host substrates, such as the extracellular matrix or eukaryotic cells, by virtue of different surface proteins (adhesins). Recently, we identified a 60-kDa cell-secreted extracellular adherence protein (Eap) of S. aureus strain Newman with broad-spectrum binding characteristics (M. Palma, A. Haggar, and J. I. Flock, J. Bacteriol. 181:2840-2845, 1999), and we have molecularly confirmed Eap to be an analogue of the previously identified major histocompatibility complex class II analog protein (Map) (M. Hussain, K. Becker, C. von Eiff, G. Peter, and M. Herrmann, Clin. Diagn. Lab. Immunol. 8:1281-1286, 2001). Previous analyses of the Eap/Map function performed with purified protein did not allow dissection of its precise role in the complex situation of the staphylococcal whole cell presenting several secreted and wall-bound adhesins. Therefore, the role of Eap was investigated by constructing a stable eap::ermB deletion in strain Newman and by complementation of the mutant. Patterns of extracted cell surface proteins analyzed both by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and by Western ligand assays with various adhesive matrix molecules clearly confirmed the absence of Eap in the mutant. However, binding and adhesion tests using whole staphylococcal cells demonstrated that both the parent and mutant strains bound equally well to fibronectin- and fibrinogen-coated surfaces, possibly due to their recognition by other staphylococcal adhesins. Furthermore, Eap mediated staphylococcal agglutination of both wild-type and mutant cells. In contrast, the mutant adhered to a significantly lesser extent to cultured fibroblasts (P < 0.001) than did the wild type, while adherence was restorable upon complementation. Furthermore, adherence to both epithelial cells (P < 0.05) and fibroblasts (not significant) could be blocked with antibodies against Eap, whereas preimmune serum was not active. In conclusion, Eap may contribute to pathogenicity by promoting adhesion of whole staphylococcal cells to complex eukaryotic substrates.
机译：要启动侵袭性感染，金黄色葡萄球菌必须依靠不同的表面蛋白（粘附素）粘附在宿主基质上，例如细胞外基质或真核细胞。最近，我们鉴定了 S的60 kDa细胞分泌的细胞外粘附蛋白（Eap）。具有广谱结合特性的金黄色葡萄球菌纽曼菌株（M. Palma，A. Haggar，和JI Flock，J. Bacteriol。181：2840-2845，1999），并且我们在分子上证实Eap是其的类似物先前鉴定的主要组织相容性复合物II类主要相似蛋白（Map）（M. Hussain，K.Becker，C.von Eiff，G.Peter和M.Herrmann，Clin.Diagn.Lab.Immunol.8：1281-1286， 2001）。先前对用纯化蛋白进行的Eap / Map功能的分析不允许分解其在葡萄球菌全细胞呈现几种分泌型和壁结合型粘附素的复杂情况下的确切作用。因此，通过在Newman菌株中构建稳定的 eap :: ermB 缺失并通过突变体的互补来研究Eap的作用。通过十二烷基硫酸钠-聚丙烯酰胺凝胶电泳和通过Western配体分析与各种粘附基质分子分析的提取的细胞表面蛋白的模式清楚地证实了突变体中不存在Eap。然而，使用整个葡萄球菌细胞的结合和粘附测试表明，亲本菌株和突变菌株均与纤连蛋白和纤维蛋白原包被的表面结合得很好，这可能是由于它们被其他葡萄球菌粘附素识别所致。此外，Eap介导了野生型和突变型细胞的葡萄球菌凝集。相比之下，该突变体对培养的成纤维细胞的粘附程度要明显低于野生型（ P <0.001），而互补作用则可以恢复。此外，抗Eap抗体可阻断对上皮细胞（ P <0.05）和成纤维细胞（不显着）的粘附，而免疫前血清则不活跃。总之，Eap可能通过促进整个葡萄球菌细胞粘附于复杂的真核生物底物而促进致病性。

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