Okuda Ken-Ichi, Nagahori Ryuichi, Yamada Satomi, Sugimoto Shinya, Sato Chikara, Sato Mari, Iwase Tadayuki, Hashimoto Kazuhiro, Mizunoe Yoshimitsu
Department of Bacteriology, The Jikei University School of Medicine, Tokyo, Japan.
Jikei Center for Biofilm Science and Technology, Tokyo, Japan.
Front Microbiol. 2018 Feb 14;9:182. doi: 10.3389/fmicb.2018.00182. eCollection 2018.
The present study aimed to understand the biofilm formation mechanism of by analyzing the components and structure of the biofilms. strains were isolated from the surface of explanted cardiac pacemaker devices that exhibited no clinical signs of infection. Culture tests using a simple stamp culture method (pressing pacemakers against the surface of agar plates) revealed frequent colonization on the surface of cardiac pacemaker devices. . was isolated from 7/31 devices, and the isolates were categorized by multilocus sequence typing into five different sequence types (STs): ST4 (JK18.2), ST53 (JK17.1), ST69 (JK12.2 and JK13.1), ST124 (JK5.3), ST125 (JK6.2), and unknown ST (JK19.3). An biofilm formation assay using microtiter plates demonstrated that 5/7 isolates formed biofilms. Inhibitory effects of DNase I and proteinase K on biofilm formation varied among isolates. In contrast, dispersin B showed no inhibitory activity against all isolates. Three-dimensional live/dead imaging of biofilms with different biochemical properties using confocal laser microscopy demonstrated different distributions and proportions of living and dead cells. Additionally, it was suggested that extracellular DNA (eDNA) plays a role in the formation of biofilms containing living cells. Ultrastructural analysis of biofilms using a transmission electron microscope and atmospheric scanning electron microscope revealed leakage of cytoplasmic components along with cell lysis and fibrous structures of eDNA connecting cells. In conclusion, the biochemical properties and structures of the biofilms differed among isolates. These findings may provide clues for establishing countermeasures against biofilm-associated infection by .
本研究旨在通过分析生物膜的组成和结构来了解[细菌名称]的生物膜形成机制。[细菌名称]菌株是从无感染临床症状的植入式心脏起搏器装置表面分离得到的。使用简单的压印培养法（将起搏器压在琼脂平板表面）进行培养测试，结果显示心脏起搏器装置表面频繁出现[细菌名称]定植。从31个装置中的7个分离出了[细菌名称]，通过多位点序列分型将分离株分为五种不同的序列类型（STs）：ST4（JK18.2）、ST53（JK17.1）、ST69（JK12.2和JK13.1）、ST124（JK5.3）、ST125（JK6.2）以及未知ST（JK19.3）。使用微量滴定板进行的[细菌名称]生物膜形成试验表明，7个分离株中有5个形成了生物膜。DNase I和蛋白酶K对生物膜形成的抑制作用在不同分离株中有所不同。相比之下，分散素B对所有分离株均无抑制活性。使用共聚焦激光显微镜对具有不同生化特性的[细菌名称]生物膜进行三维活/死成像，结果显示活细胞和死细胞的分布及比例不同。此外，有研究表明细胞外DNA（eDNA）在含活细胞的生物膜形成中发挥作用。使用透射电子显微镜和常压扫描电子显微镜对[细菌名称]生物膜进行超微结构分析，结果显示细胞质成分泄漏，同时伴有细胞裂解以及连接细胞的eDNA纤维结构。总之，不同[细菌名称]分离株的生物膜生化特性和结构存在差异。这些发现可能为制定针对[细菌名称]相关生物膜感染的应对措施提供线索。
