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The Surface Protein Pls of Methicillin-Resistant Staphylococcus aureus Is a Virulence Factor in Septic Arthritis

机译:耐甲氧西林金黄色葡萄球菌的表面蛋白Pls是化脓性关节炎的致病因子。

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摘要

Pls, a surface protein of certain methicillin-resistant Staphylococcus aureus strains, is associated with poor bacterial adherence to solid-phase fibronectin and immunoglobulin G, as well as with reduced invasion of cultured epithelial cells. Here the importance of Pls for the development of septic arthritis and sepsis was investigated by using a mouse model. Mice inoculated with a pls knockout mutant developed a much milder arthritis and showed less grave weight reduction than mice infected with the wild-type Pls+ clinical isolate. Also, the pls mutant induced a significantly lower frequency of mortality than the wild-type strain. The bacterial load of the kidneys was larger in mice infected with the Pls+ strain than in animals challenged with the pls mutant. However, there was no evident inflammatory effect due to the Pls molecule alone, as indicated by knee injection of purified Pls. In conclusion, the results show that Pls is a virulence factor for septic arthritis and sepsis.
机译:Pl是某些耐甲氧西林金黄色葡萄球菌菌株的表面蛋白,与细菌对固相纤连蛋白和免疫球蛋白G的粘附力差以及培养的上皮细胞的侵袭减少有关。在这里,通过使用小鼠模型研究了Pl对于败血性关节炎和败血症发展的重要性。与野生型Pls + 临床分离株感染的小鼠相比,接种pls基因敲除突变体的小鼠患上的关节炎要轻得多,并且体重减轻得更少。而且,pls突变体引起的死亡率显着低于野生型菌株。感染Pls + 菌株的小鼠的肾脏的细菌载量大于用pls突变体攻击的动物的肾脏。然而,如膝注射纯化的P1s所表明的,没有单独的P1s分子引起的明显的炎症作用。总之,结果表明,Pls是脓毒性关节炎和败血症的致病因子。

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