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.

该副本是利用资源的众多研究子项目之一 由NIH/NCRR资助的中心赠款提供。对该子弹的主要支持 而且，副投影的主要研究员可能是其他来源提供的 包括其他NIH来源。 列出的总费用可能 代表subproject使用的中心基础架构的估计量， NCRR赠款不直接向子弹或副本人员提供的直接资金。 该项目的目的是阐明铜（CU）表面施加的应力的细胞靶标。在这项工作之前，尚不清楚Cu表面的抗菌特性是否与细胞壁或膜损伤直接相关，释放含有Cu摄取的Cu离子和细胞的铜中毒。或者，潜在的机制可能是遗传物质的降解，或者细菌因CU引起的间接氧化事件而死亡。具体来说，该项目研究了以下Cu表面应力的潜在模式：（i）膜损伤，（ii）DNA和（iii）氧化损伤的诱变。 为了解决这些问题，我们采取了两种独立策略： 目标1：确定控制细菌灭活的分子靶标，例如大肠杆菌和真菌，例如酿酒酵母的酵母菌糖含量或金属铜表面上的白色念珠菌。 AIM 2：确定负责抵抗金属铜表面的遗传因素。 总体而言，这些研究改善了我们对Cu表面介导的毒性和金属Cu抗菌作用模式的理解。