LPS (lipopolysaccharide, endotoxin) susceptibility, an important factor in the innate immune response to Gram-negative bacterial infections. Benefits and hazards of LPS hypersensitivity
LPS(脂多糖,内毒素)敏感性,是对革兰氏阴性细菌感染的先天免疫反应的重要因素。
基本信息
- 批准号:5356930
- 负责人:
- 金额:--
- 依托单位:
- 依托单位国家:德国
- 项目类别:Priority Programmes
- 财政年份:2002
- 资助国家:德国
- 起止时间:2001-12-31 至 2007-12-31
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
LPS (lipopolysaccharide, endotoxin) is a major component of the outer cell wall of Gram-negative bacteria. LPS plays an important role in the early recognition and in the defense against invading bacteria by the innate immune system. The activation of the innate immune system however, is not without complications for the infected organism. LPS is a potent inducer of many pathophysiological activities seen during infection, including the development of endotoxin shock, frequently with lethal outcome. With the proposed research project it is intended to make a useful contribution to the clarifying of genetic factors determining innate LPS susceptibility and to the understanding of the factors underlying the development of LPS hypersensitivity and its role in the course of infection. The objectives of the study are the following: A. To obtain definite evidence that TLR4 (Toll-like receptor 4) is the central recognition and signaling protein in the activation of cells by LPS. B. To study the involvement of IFN (Interferon)-a/b in the induction of IFN-g and thus in the induction of LPS hypersensitivity in infected host. The pathogen-induced IFN-g represents the key mediator of LPS hypersensitivity that develops during infection. C. To investigate the consequences of an existing LPS hypersensitivity on 1) the resistance to infection and 2) the risk of development of endotoxin shock. Both properties result from an activation of the innate immune system by LPS.
LPS(脂多糖,内毒素)是革兰氏阴性细菌外细胞壁的主要组成部分。 LPS在早期认可和防御先天免疫系统入侵细菌的辩护中起着重要作用。但是,先天免疫系统的激活对于感染生物并非并非并发症。 LPS是感染过程中观察到的许多病理生理活性的有效诱导剂,包括内毒素休克的发展,经常以致命的结局。通过拟议的研究项目,旨在为阐明决定先天有限责任的易感性以及对LPS超敏反应发展的因素的理解及其在感染过程中的作用的理解做出有用的贡献。该研究的目的是:A。获得确定的证据,表明TLR4(Toll样受体4)是LPS激活细胞中的中心识别和信号蛋白。 B.研究IFN(干扰素)-a/b参与IFN-G的诱导,从而在感染宿主中诱导LPS超敏反应。病原体诱导的IFN-G代表了感染过程中LPS超敏反应的关键介体。 C.研究现有LPS超敏反应对1)感染的耐药性和2)内毒素休克的风险的后果。这两种特性都是由LPS先天免疫系统激活引起的。
项目成果
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Professorin Dr. Marina Alexandra Freudenberg其他文献
Professorin Dr. Marina Alexandra Freudenberg的其他文献
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