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在小鼠装置相关感染模型中,主要自溶素对金黄色葡萄球菌USA300 LAC JE2的毒力来说是多余的。

The major autolysin is redundant for Staphylococcus aureus USA300 LAC JE2 virulence in a murine device-related infection model.

作者信息

McCarthy Hannah, Waters Elaine M, Bose Jeffrey L, Foster Simon, Bayles Kenneth W, O'Neill Eoghan, Fey Paul D, O'Gara James P

机构信息

Department of Microbiology, School of Natural Sciences, National University of Ireland, Galway, Ireland.

Department of Pathology and Microbiology, Center for Staphylococcal Research, University of Nebraska Medical Center, Omaha, NE 68198-5900, USA.

出版信息

FEMS Microbiol Lett. 2016 May;363(9). doi: 10.1093/femsle/fnw087. Epub 2016 Apr 3.

DOI:10.1093/femsle/fnw087
PMID:27044299
Abstract

The major Staphylococcus aureus autolysin, Atl, has been implicated in attachment to surfaces and release of extracellular DNA during biofilm formation under laboratory conditions. Consistent with this, polyclonal antibodies to the amidase and glucosaminidase domains of Atl inhibited in vitro biofilm formation. However, in a murine model of device-related infection the community-associated S. aureus strain USA300 LAC JE2 established a successful infection in the absence of atl These data indicate that Atl activity is not required for biofilm production in this infection model and reveal the importance of characterizing the contribution of biofilm phenotypes to virulence under in vivo conditions.

摘要

金黄色葡萄球菌的主要自溶素Atl,在实验室条件下的生物膜形成过程中,与表面附着及细胞外DNA释放有关。与此一致的是,针对Atl酰胺酶和葡糖胺酶结构域的多克隆抗体可抑制体外生物膜形成。然而,在与装置相关感染的小鼠模型中,社区获得性金黄色葡萄球菌菌株USA300 LAC JE2在缺失atl的情况下仍成功建立感染。这些数据表明,在该感染模型中生物膜产生并不需要Atl活性,并揭示了在体内条件下表征生物膜表型对毒力贡献的重要性。

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