MODE OF ACTION OF REDOX-ACTIVE COPPER SURFACES AGAINST MICROBES

氧化还原活性铜表面对抗微生物的作用方式

• 批准号: 8360528
• 负责人: GREGOR GRASS
• 金额: $ 6.72万
• 依托单位: UNIVERSITY OF NEBRASKA LINCOLN
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-08-01 至 2012-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8360528
• 关键词: Address; Bacteria; Biology; Candida albicans; Cell Wall; Cell membrane; Cells; Copper; DNA; Escherichia coli; Event; Funding; Genetic; Genetic Materials; Goals; Grant; Ions; Mediating; Membrane; Microbe; Molecular Target; National Center for Research Resources; Oxidation-Reduction; Principal Investigator; Property; Research; Research Infrastructure; Resistance; Resources; Saccharomyces cerevisiae; Source; Stress; Surface; Toxic effect; United States National Institutes of Health; Work; Yeasts; antimicrobial; cellular targeting; copper poisoning; cost; fungus; improved; oxidative damage; uptake

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. The goal of this project was to elucidate the cellular targets of stress exerted by copper (Cu) surfaces. Prior to this work it was not known if the antimicrobial properties of Cu surfaces are directly related to cell wall or membrane damage, release of Cu ions with concomitant Cu uptake and copper poisoning of the cells. Alternatively, the underlying mechanisms could be degradation of genetic material or that bacteria die by indirect oxidative events caused by Cu. Specifically the following potential modes of Cu surface stress were investigated in this project: (i) membrane damage, (ii) mutagenicity of DNA and (iii) oxidative damage. To address these questions we have pursued two independent strategies: Aim 1: Identify the molecular targets that govern inactivation of bacteria such as Escherichia coli and fungi such as the yeasts Saccharomyces cerevisiae or Candida albicans on metallic Cu surfaces. Aim 2: Identify genetic factors responsible for resistance against metallic copper surfaces. Overall, these studies have improved our understanding of Cu surface mediated toxicity and of the underlying mode of antimicrobial action of metallic Cu.

该子项目是利用资源的众多研究子项目之一 由 NIH/NCRR 资助的中心拨款提供。子项目的主要支持 并且子项目的首席研究员可能是由其他来源提供的， 包括其他 NIH 来源。 子项目可能列出的总成本 代表子项目使用的中心基础设施的估计数量， NCRR 赠款不直接向子项目或子项目工作人员提供资金。 该项目的目标是阐明铜 (Cu) 表面施加的应力的细胞目标。在这项工作之前，尚不清楚铜表面的抗菌特性是否与细胞壁或膜损伤、铜离子的释放以及铜的吸收和细胞的铜中毒直接相关。或者，潜在的机制可能是遗传物质的降解或细菌因铜引起的间接氧化事件而死亡。具体而言，本项目研究了铜表面应力的以下潜在模式：(i) 膜损伤，(ii) DN​​A 致突变性和 (iii) 氧化损伤。 为了解决这些问题，我们采取了两种独立的策略： 目标 1：确定金属铜表面上控制细菌（如大肠杆菌）和真菌（如酿酒酵母或白色念珠菌）失活的分子靶点。 目标 2：确定导致金属铜表面耐受性的遗传因素。 总的来说，这些研究提高了我们对铜表面介导的毒性和金属铜抗菌作用的潜在模式的理解。