• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Infection and immunity >Use of a Human-Like Low-Grade Bacteremia Model of Experimental Endocarditis To Study the Role of Staphylococcus aureus Adhesins and Platelet Aggregation in Early Endocarditis
【24h】

Use of a Human-Like Low-Grade Bacteremia Model of Experimental Endocarditis To Study the Role of Staphylococcus aureus Adhesins and Platelet Aggregation in Early Endocarditis

机译：实验性心内膜炎类似人的低度细菌血症模型的使用，以研究金黄色葡萄球菌粘附素和血小板聚集在早期心内膜炎中的作用

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Animal models of infective endocarditis (IE) induced by high-grade bacteremia revealed the pathogenic roles of Staphylococcus aureus surface adhesins and platelet aggregation in the infection process. In humans, however, S. aureus IE possibly occurs through repeated bouts of low-grade bacteremia from a colonized site or intravenous device. Here we used a rat model of IE induced by continuous low-grade bacteremia to explore further the contributions of S. aureus virulence factors to the initiation of IE. Rats with aortic vegetations were inoculated by continuous intravenous infusion (0.0017 ml/min over 10 h) with 106 CFU of Lactococcus lactis pIL253 or a recombinant L. lactis strain expressing an individual S. aureus surface protein (ClfA, FnbpA, BCD, or SdrE) conferring a particular adhesive or platelet aggregation property. Vegetation infection was assessed 24 h later. Plasma was collected at 0, 2, and 6 h postinoculation to quantify the expression of tumor necrosis factor (TNF), interleukin 1α (IL-1α), IL-1β, IL-6, and IL-10. The percentage of vegetation infection relative to that with strain pIL253 (11%) increased when binding to fibrinogen was conferred on L. lactis (ClfA strain) (52%; P = 0.007) and increased further with adhesion to fibronectin (FnbpA strain) (75%; P < 0.001). Expression of fibronectin binding alone was not sufficient to induce IE (BCD strain) (10% of infection). Platelet aggregation increased the risk of vegetation infection (SdrE strain) (30%). Conferring adhesion to fibrinogen and fibronectin favored IL-1β and IL-6 production. Our results, with a model of IE induced by low-grade bacteremia, resembling human disease, extend the essential role of fibrinogen binding in the initiation of S. aureus IE. Triggering of platelet aggregation or an inflammatory response may contribute to or promote the development of IE.
机译：高度菌血症诱导的感染性心内膜炎（IE）的动物模型揭示了金黄色葡萄球菌表面粘附素和血小板聚集在感染过程中的致病作用。但是，在人类中，金黄色葡萄球菌IE可能是通过从定居点或静脉内装置反复发作低度菌血症而发生的。在这里，我们使用连续低度菌血症诱导的IE大鼠模型进一步探讨金黄色葡萄球菌毒力因子对IE引发的贡献。用10 6 CFU的乳酸乳球菌 pIL253或重组的 L连续静脉输注（10小时内0.0017 ml / min，共10次）接种主动脉植被的大鼠。表达单个金黄色葡萄球菌表面蛋白（ClfA，FnbpA，BCD或SdrE）的乳酸菌菌株，具有特殊的黏附或血小板聚集特性。 24小时后评估植被感染。接种后0、2和6小时收集血浆，以量化肿瘤坏死因子（TNF），白介素1α（IL-1α），IL-1β，IL-6和IL-10的表达。当与 L赋予纤维蛋白原结合时，相对于pIL253菌株，植被感染的百分比增加（11％）。乳酸（ClfA菌株）（52％; P = 0.007），并随着与纤连蛋白（FnbpA菌株）的粘附而进一步增加（75％; P <0.001） 。单独表达纤连蛋白的结合不足以诱导IE（BCD株）（感染的10％）。血小板聚集增加了植物感染（SdrE株）的风险（30％）。赋予与纤维蛋白原和纤连蛋白的粘附性有利于IL-1β和IL-6的产生。我们的结果，类似于人类疾病，由低度菌血症诱导的IE模型，扩展了纤维蛋白原结合在金黄色葡萄球菌IE引发中的重要作用。触发血小板聚集或炎症反应可能有助于或促进IE的发展。

著录项

相似文献

  • 外文文献
  • 中文文献
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号