The ability of biofilm formation does not influence virulence of Staphylococcus aureus and host response in a mouse tissue cage infection model

被引:52
|
作者
Kristian, SA
Golda, T
Ferracin, F
Cramton, SE
Neumeister, B
Peschel, A
Götz, F
Landmann, R
机构
[1] Univ Basel Hosp, Dept Res, Div Infect Dis, CH-4031 Basel, Switzerland
[2] Univ Tubingen, D-72076 Tubingen, Germany
[3] Univ Tubingen Hosp, Dept Transfus Med, D-72076 Tubingen, Germany
[4] Univ Tubingen Hosp, Dept Surg, D-72076 Tubingen, Germany
[5] Univ Tubingen Hosp, Dept Med Microbiol & Hyg, D-72076 Tubingen, Germany
关键词
Staphylococcus aureus; polysaccharide intercellular adhesin; ica operon; biofilm; virulence; tissue cage infection model;
D O I
10.1016/j.micpath.2003.12.004
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The virulence of Staphylococcus aureus Sal 13 (SA 113) 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. (C) 2004 Elsevier Ltd. All rights reserved.
引用
收藏
页码:237 / 245
页数:9
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