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粪肠球菌OG1RF的gls24突变体在实验性心内膜炎模型中的毒力降低。

Decreased virulence of a gls24 mutant of Enterococcus faecalis OG1RF in an experimental endocarditis model.

作者信息

Nannini Esteban C, Teng Fang, Singh Kavindra V, Murray Barbara E

机构信息

Center for the Study of Emerging and Re-Emerging Pathogens, University of Texas Medical School at Houston, 6431 Fannin, MSB 2.112, Houston, TX 77030, USA.

出版信息

Infect Immun. 2005 Nov;73(11):7772-4. doi: 10.1128/IAI.73.11.7772-7774.2005.

Abstract

In the current study, the gls24 disruption mutant TX10100, previously shown to be more sensitive to bile salts and attenuated in a mouse peritonitis model, showed an approximately fivefold higher 50% infective dose than wild-type OG1RF in a rat endocarditis model. When administered as a mixture, TX10100, unlike a downstream glsB mutant, was significantly outnumbered by OG1RF in vegetations, organs, and blood, despite being inoculated in greater numbers. These results indicate that gls24 is important in the pathogenesis of enterococcal endocarditis.

摘要

在当前研究中,gls24缺失突变体TX10100此前已显示对胆盐更敏感且在小鼠腹膜炎模型中毒力减弱,在大鼠心内膜炎模型中其半数感染剂量比野生型OG1RF高约五倍。当作为混合物给药时,与下游glsB突变体不同,尽管TX10100接种数量更多,但在赘生物、器官和血液中其数量却被OG1RF显著超过。这些结果表明gls24在肠球菌心内膜炎的发病机制中起重要作用。

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