Kristian Sascha A, Golda Thomas, Ferracin Fabrizia, Cramton Sarah E, Neumeister Birgid, Peschel Andreas, Götz Friedrich, Landmann Regine
Microbial Genetics, University of Tübingen, 72076 Tübingen, Germany.
Microb Pathog. 2004 May;36(5):237-45. doi: 10.1016/j.micpath.2003.12.004.
The virulence of Staphylococcus aureus Sa113 (SA113) and an isogenic ica deletion mutant (ica-), deficient in the production of polysaccharide intercellular adhesin (PIA), which is crucial for biofilm formation, was compared in a mouse tissue cage infection model. The minimal infective doses for the induction of persistent tissue infections in C57BL/6 mice were 10(3) CFU for both SA113 and the ica- mutant. Bacterial growth, initial adherence to surfaces within the implants and the course of inflammation including growth-dependent host TNF and MIP-2 release, influx of phagocytes and an accumulation of dead leukocytes were similar as well. Since SA113 expressed PIA in vivo, we could demonstrate that PIA and the lack of biofilm formation did not influence the capacity of S. aureus to induce persistent infections and did not modulate host responses in the mouse tissue cage model.
在小鼠组织笼感染模型中，比较了金黄色葡萄球菌Sa113（SA113）和同基因ica缺失突变体（ica-）的毒力。ica-缺乏对生物膜形成至关重要的胞间多糖黏附素（PIA）的产生。SA113和ica-突变体在C57BL/6小鼠中诱导持续性组织感染的最小感染剂量均为10³CFU。细菌生长、对植入物内表面的初始黏附以及炎症过程，包括生长依赖性宿主肿瘤坏死因子（TNF）和巨噬细胞炎性蛋白-2（MIP-2）释放、吞噬细胞流入和死亡白细胞积聚，也都相似。由于SA113在体内表达PIA，我们可以证明PIA和生物膜形成的缺乏并不影响金黄色葡萄球菌诱导持续性感染的能力，也不会在小鼠组织笼模型中调节宿主反应。
