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Intracellular survival determinants of Yersinia pestis

Intracellular survival determinants of Yersinia pestis
鼠疫耶尔森氏菌的细胞内生存决定因素
批准号:
6511514
负责人:
James B Bliska
金额:
$7.53万
依托单位国家:
美国
项目类别:
财政年份:
2001
资助国家:
美国
项目状态:
已结题
起止时间:
2001-07-01 至 2004-06-30

项目摘要

项目成果

James B Bliska的其他基金

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中文摘要
翻译
描述(由申请人提供):鼠疫耶尔森氏菌是鼠疫的病原体, 一种急性的,通常是致命的细菌感染,通过跳蚤叮咬传播, 气雾剂Y.鼠疫被认为是一种兼性细胞内病原体。 以往的数据表明,Y.鼠疫菌生存和复制 巨噬细胞在感染的最初几个小时,而细胞外 生长在较晚的时间点占主导地位。Y.鼠疫 在巨噬细胞中存活和复制是未知的。长期目标 的建议研究是确定分子和细胞的基础, 胞内存活率。巨噬细胞中的鼠疫为了实现这一目标,我们 将(1)表征巨噬细胞防御是重要的限制 细胞内存活和复制。鼠疫菌;(2)确定 Y.鼠疫杆菌,这是重要的打击细胞内防御, 巨噬细胞了解Y.鼠疫 可能有助于开发预防或治疗鼠疫感染的新方法, 人类人口。
英文摘要
DESCRIPTION (provided by applicant): Yersinia pestis is the agent of plague, an acute, often fatal bacterial infection that is transmitted by flea bite or aerosol. Y. pestis is considered to be a facultative intracellular pathogen. Previous data indicate that Y. pestis survives and replicates within macrophages during the first few hours of infection, while extracellular growth is predominant at later time points. The mechanism by which Y. pestis survives and replicates in macrophages is not known. The long-term objective of the proposed studies is to determine the molecular and cellular basis for intracellular survival of Y. pestis in macrophages. To achieve this goal we will (1) Characterize macrophage defenses that are important for limiting intracellular survival and replication of Y. pestis; and (2) Identify genes in Y. pestis that are important for combating intracellular defenses of macrophages. Understanding the intracellular survival mechanism of Y. pestis may aid the development of new ways to prevent or treat plague infections in the human population.
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Regulation of host innate and adaptive immunity by bacterial type III effectors
  • 批准号:
    9898220
  • 项目类别:
  • 资助金额:
    $36.55万
  • 财政年份:
    2012
  • 负责人:
    James B Bliska
  • 依托单位:
Regulation of host innate and adaptive immunity by bacterial type III effectors
Regulation of host innate and adaptive immunity by bacterial type III effectors
Regulation of host innate and adaptive immunity by bacterial type III effectors