Bacterial Interference to Prevent Staphylococcus aureus Infection

预防金黄色葡萄球菌感染的细菌干扰

基本信息

  • 批准号:
    10241299
  • 负责人:
  • 金额:
    $ 41.75万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2018
  • 资助国家:
    美国
  • 起止时间:
    2018-09-05 至 2023-08-31
  • 项目状态:
    已结题

项目摘要

PROJECT SUMMARY Although Staphylococcus aureus is a major human pathogen that causes an enormous burden of disease, we have very few strategies for preventing infection or controlling its spread. In the 1960's it was a widespread practice to inoculate neonates with a relatively benign strain of S. aureus called 502A as a strategy to combat outbreaks of more virulent staphylococcal strains, a practice referred to as bacterial interference. Thousands of neonates were exposed to 502A with very little associated morbidity and mortality, but despite its relatively good safety record, the practice was abandoned in the 1970's due to safety concerns. The basic mechanisms of bacterial interference were never investigated. We recently showed that 502A elicits a very different cytokine response compared to other epidemic and virulent strains. Although it is less invasive, host cells exposed to 502A have increased levels of type I Interferons as well as several other proinflammatory cytokines (eg., TNFa, IL-6) compared to exposure to other S. aureus strains. Our hypothesis is that S. aureus strains that stimulate 502A-like immune responses protect from colonization and subsequent infection by inducing the immune system to reject other strains. Understanding the mechanism of 502A bacterial interference could allow us to design strategies for protection against colonization and infection with virulent or antibiotic resistant strains. It may also lead to strategies for decolonization in the setting of recurrent S. aureus infection or in intensive care units where universal decolonization using antimicrobials has been show to decrease mortality. We combine a clinical approach with basic molecular research, aiming to assess the feasibility of a bacterial interference strategy in the clinical context. The study team integrates expertise in clinical S. aureus epidemiology, host innate immunology, and genomics and microbiome studies. Aim 1 uses the natural diversity in S. aureus strains found in human populations to prospectively assess the correlation of colonization with 502A-like strains and possible protection. Aim 2 uses model systems to assess the response of the immune system to 502A-like strains as well as their protective effect. Aim 3 examines the possibility of using a virulence-attenuated strain for bacterial interference and decolonization.
项目摘要 虽然金黄色葡萄球菌是一种主要的人类病原体, 由于疾病负担,我们几乎没有预防感染或控制其 传播.在20世纪60年代,普遍的做法是用相对较低的 良性S.金黄色葡萄球菌称502 A是一项战略,以打击爆发更多的 毒性葡萄球菌菌株,这种做法被称为细菌干扰。 数千名新生儿暴露于502 A,几乎没有相关的发病率, 死亡率,但尽管其相对良好的安全记录,实践中被放弃, 1970年,出于安全考虑。细菌干扰的基本机制是 从未调查过。我们最近发现,502 A激发了一种非常不同的细胞因子, 与其他流行病和强毒株相比,虽然它的侵入性较小, 暴露于502 A的宿主细胞具有增加的I型干扰素水平以及几种 其它促炎细胞因子(例如,TNF α,IL-6)相比,暴露于其他S. 金黄色葡萄球菌我们假设S.刺激502 A样的金黄色葡萄球菌菌株 免疫应答通过以下方式保护免于定植和随后的感染: 诱导免疫系统排斥其他菌株。了解机制 502 A细菌干扰可以让我们设计策略, 定植和感染毒性或抗生素抗性菌株。还可能导致 非殖民化战略的设置经常性的S。金黄色葡萄球菌感染或 使用抗菌剂进行普遍去殖民化的护理单位已被证明, 降低死亡率。我们联合收割机将临床方法与基础分子研究相结合, 旨在评估细菌干扰策略在临床环境中的可行性。 该研究小组整合了临床S。金黄色葡萄球菌流行病学,宿主先天性 免疫学、基因组学和微生物组学研究。目标1利用自然多样性, S.在人群中发现的金黄色葡萄球菌菌株,以前瞻性地评估 502 A样菌株的定殖和可能的保护。目标2使用模型系统 为了评估免疫系统对502 A样菌株的反应以及它们的 保护作用。目的3检验使用毒力减毒菌株的可能性 进行细菌干扰和去殖民化。

项目成果

期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)

数据更新时间:{{ journalArticles.updateTime }}

{{ item.title }}
{{ item.translation_title }}
  • DOI:
    {{ item.doi }}
  • 发表时间:
    {{ item.publish_year }}
  • 期刊:
  • 影响因子:
    {{ item.factor }}
  • 作者:
    {{ item.authors }}
  • 通讯作者:
    {{ item.author }}

数据更新时间:{{ journalArticles.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ monograph.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ sciAawards.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ conferencePapers.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ patent.updateTime }}

PAUL J PLANET其他文献

PAUL J PLANET的其他文献

{{ item.title }}
{{ item.translation_title }}
  • DOI:
    {{ item.doi }}
  • 发表时间:
    {{ item.publish_year }}
  • 期刊:
  • 影响因子:
    {{ item.factor }}
  • 作者:
    {{ item.authors }}
  • 通讯作者:
    {{ item.author }}

{{ truncateString('PAUL J PLANET', 18)}}的其他基金

In Host Evolution of Nontuberculous Mycobacteria in Cystic Fibrosis
囊性纤维化中非结核分枝杆菌的宿主进化
  • 批准号:
    9896274
  • 财政年份:
    2020
  • 资助金额:
    $ 41.75万
  • 项目类别:
In Host Evolution of Nontuberculous Mycobacteria in Cystic Fibrosis
囊性纤维化中非结核分枝杆菌的宿主进化
  • 批准号:
    10092929
  • 财政年份:
    2020
  • 资助金额:
    $ 41.75万
  • 项目类别:
Role of Staphylococcus aureus SpA in Microbial Competition and Host Colonization
金黄色葡萄球菌 SpA 在微生物竞争和宿主定殖中的作用
  • 批准号:
    8685117
  • 财政年份:
    2012
  • 资助金额:
    $ 41.75万
  • 项目类别:
Role of Staphylococcus aureus SpA in Microbial Competition and Host Colonization
金黄色葡萄球菌 SpA 在微生物竞争和宿主定殖中的作用
  • 批准号:
    8508186
  • 财政年份:
    2012
  • 资助金额:
    $ 41.75万
  • 项目类别:
Role of Staphylococcus aureus SpA in Microbial Competition and Host Colonization
金黄色葡萄球菌 SpA 在微生物竞争和宿主定殖中的作用
  • 批准号:
    8353993
  • 财政年份:
    2012
  • 资助金额:
    $ 41.75万
  • 项目类别:

相似海外基金

Ecological and Evolutionary Drivers of Antibiotic Resistance in Patients
患者抗生素耐药性的生态和进化驱动因素
  • 批准号:
    EP/Y031067/1
  • 财政年份:
    2024
  • 资助金额:
    $ 41.75万
  • 项目类别:
    Research Grant
Collaborative Research: Leveraging the interactions between carbon nanomaterials and DNA molecules for mitigating antibiotic resistance
合作研究:利用碳纳米材料和 DNA 分子之间的相互作用来减轻抗生素耐药性
  • 批准号:
    2307222
  • 财政年份:
    2024
  • 资助金额:
    $ 41.75万
  • 项目类别:
    Standard Grant
Molecular Epidemiology of Antibiotic Resistance in Clostridioides difficile
艰难梭菌抗生素耐药性的分子流行病学
  • 批准号:
    502587
  • 财政年份:
    2024
  • 资助金额:
    $ 41.75万
  • 项目类别:
Collaborative Research: Leveraging the interactions between carbon nanomaterials and DNA molecules for mitigating antibiotic resistance
合作研究:利用碳纳米材料和 DNA 分子之间的相互作用来减轻抗生素耐药性
  • 批准号:
    2307223
  • 财政年份:
    2024
  • 资助金额:
    $ 41.75万
  • 项目类别:
    Standard Grant
The roles of a universally conserved DNA-and RNA-binding domain in controlling MRSA virulence and antibiotic resistance
普遍保守的 DNA 和 RNA 结合域在控制 MRSA 毒力和抗生素耐药性中的作用
  • 批准号:
    MR/Y013131/1
  • 财政年份:
    2024
  • 资助金额:
    $ 41.75万
  • 项目类别:
    Research Grant
Determining structural dynamics of membrane proteins in their native environment: focus on bacterial antibiotic resistance
确定膜蛋白在其天然环境中的结构动力学:关注细菌抗生素耐药性
  • 批准号:
    MR/X009580/1
  • 财政年份:
    2024
  • 资助金额:
    $ 41.75万
  • 项目类别:
    Fellowship
CAREER: Systems Microbiology and InterdiscipLinary Education for Halting Environmental Antibiotic Resistance Transmission (SMILE HEART)
职业:阻止环境抗生素耐药性传播的系统微生物学和跨学科教育(SMILE HEART)
  • 批准号:
    2340818
  • 财政年份:
    2024
  • 资助金额:
    $ 41.75万
  • 项目类别:
    Continuing Grant
Reinforcing the battle at the bacterial cell wall: Structure-guided characterization and inhibition of beta-lactam antibiotic resistance signalling mechanisms
加强细菌细胞壁的战斗:β-内酰胺抗生素耐药信号机制的结构引导表征和抑制
  • 批准号:
    480022
  • 财政年份:
    2023
  • 资助金额:
    $ 41.75万
  • 项目类别:
    Operating Grants
The spread of antibiotic resistance in bacteria-plasmid networks
抗生素耐药性在细菌-质粒网络中的传播
  • 批准号:
    BB/X010473/1
  • 财政年份:
    2023
  • 资助金额:
    $ 41.75万
  • 项目类别:
    Fellowship
An RNA Nanosensor for the Diagnosis of Antibiotic Resistance in M. Tuberculosis
用于诊断结核分枝杆菌抗生素耐药性的 RNA 纳米传感器
  • 批准号:
    10670613
  • 财政年份:
    2023
  • 资助金额:
    $ 41.75万
  • 项目类别:
{{ showInfoDetail.title }}

作者:{{ showInfoDetail.author }}

知道了