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多形核白细胞与金黄色葡萄球菌生物膜相互作用导致小泡形成。

Vesicle formation as a result of interaction between polymorphonuclear neutrophils and Staphylococcus aureus biofilm.

机构信息

Department of Microbiology and Immunology, Nizhny Novgorod State Medical Academy, Nizhny Novgorod, Russia.

出版信息

J Med Microbiol. 2013 Aug;62(Pt 8):1153-1159. doi: 10.1099/jmm.0.048967-0. Epub 2013 May 22.

DOI:10.1099/jmm.0.048967-0
PMID:23699065
Abstract

Staphylococcus aureus, a major opportunistic pathogen, is a leading cause of biofilm-related infections in clinical practice. Staphylococcal biofilms are highly resistant to antibacterial medicines and immune effector cells. The main result of our work is the discovery of nano-vesicles in the supernatant of the human neutrophil-S. aureus biofilm system. We also found that phospholipase C treatment causes complete destruction of these vesicles. While the addition of proteinase K led to a partial structural disorganization of the vesicles, DNase treatment did not influence the vesicle structure. These observations allowed us to conclude that phospholipids and proteins play a structure-forming role in the formation of these nano-vesicles. The vesicles demonstrated anti-biofilm activities when tested against Staphylococcus epidermidis (strains 178M and 328/5) biofilms, but were ineffective for S. aureus (strains 5983/2, 5663 and 18A) biofilms.

摘要

金黄色葡萄球菌是一种主要的机会性病原体,是临床实践中与生物膜相关感染的主要原因。葡萄球菌生物膜对抗菌药物和免疫效应细胞具有高度抗性。我们工作的主要结果是在人中性粒细胞-金黄色葡萄球菌生物膜系统的上清液中发现了纳米囊泡。我们还发现,磷脂酶 C 处理会导致这些囊泡完全破坏。虽然添加蛋白酶 K 会导致囊泡的部分结构解组织,但 DNA 酶处理不会影响囊泡结构。这些观察结果使我们得出结论,磷脂和蛋白质在这些纳米囊泡的形成中起结构形成作用。当测试对表皮葡萄球菌(菌株 178M 和 328/5)生物膜的抗生物膜活性时,这些囊泡显示出抗生物膜活性,但对金黄色葡萄球菌(菌株 5983/2、5663 和 18A)生物膜无效。

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