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Reduced adherence to traumatized rat heart valves by a low-fibronectin-binding mutant of Staphylococcus aureus.

机译:低纤连蛋白结合的金黄色葡萄球菌突变体减少了对受损伤的大鼠心脏瓣膜的依从性。

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Isogenic strains of Staphylococcus aureus, differing in fibronectin binding, were constructed for studies of the contribution of fibronectin binding to the in vivo pathogenesis of staphylococcal disease. Mutagenesis of S. aureus 879R4S was accomplished by mating with Enterococcus faecalis FA378 that carried the transposon Tn918. Four low-fibronectin-binding mutants were identified that bound 24- to 35-fold less fibronectin than the parent strain did. A spectinomycin-resistant strain, R4SSp, was transduced by a bacteriophage (80 alpha) lysate propagated on a low-binding mutant of 879R4S to produce R4SSp/1536, which bound less fibronectin, contained a single copy of the transposon, and grew on spectinomycin-containing medium. Using a rat model of endocarditis, we determined the distribution of S. aureus R4SSp and its transductant in normal and cardiac catheterized rats. Cultures of heart tissue showed that catheterized rats challenged with the fibronectin-binding parent strain had over 250-fold more organisms in the left heart than did rats challenged with the low-binding transductant. The ability to bind fibronectin had no effect on the number of S. aureus cells cultured from other tissues. These data suggest that the ability of S. aureus to bind fibronectin is an important factor in establishing adherence to damaged heart valves in vivo.
机译:构建了金黄色葡萄球菌的同基因菌株,其纤连蛋白结合不同,用于研究纤连蛋白结合对葡萄球菌疾病的体内发病机理的贡献。金黄色葡萄球菌879R4S的诱变是通过与带有转座子Tn918的粪肠球菌FA378交配完成的。鉴定出四个低纤连蛋白结合突变体,其结合纤连蛋白的亲和力比亲本菌株低24至35倍。通过在低结合突变体879R4S上繁殖的噬菌体(80 alpha)裂解物转导了一种抗大观霉素的菌株R4SSp,以产生R4SSp / 1536,其结合的纤连蛋白较少,包含转座子的一个副本,并在大观霉素上生长含介质。使用心内膜炎的大鼠模型,我们确定了正常和心脏导管插入大鼠中金黄色葡萄球菌R4SSp及其转导物的分布。心脏组织培养物显示,与纤连蛋白结合的亲本菌株攻击的导管插入大鼠在左心脏的生物比与低结合的转导子攻击的大鼠多250倍。结合纤连蛋白的能力对从其他组织培养的金黄色葡萄球菌细胞的数量没有影响。这些数据表明,金黄色葡萄球菌结合纤连蛋白的能力是在体内建立对受损心脏瓣膜的依从性的重要因素。

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