Suppr超能文献

细胞内细菌病原体感染引发的宿主代谢反应。

Metabolic host responses to infection by intracellular bacterial pathogens.

机构信息

Lehrstuhl für Biochemie, Center of Isotopologue Profiling, Technische Universität München Garching, Germany.

出版信息

Front Cell Infect Microbiol. 2013 Jul 9;3:24. doi: 10.3389/fcimb.2013.00024. eCollection 2013.

Abstract

The interaction of bacterial pathogens with mammalian hosts leads to a variety of physiological responses of the interacting partners aimed at an adaptation to the new situation. These responses include multiple metabolic changes in the affected host cells which are most obvious when the pathogen replicates within host cells as in case of intracellular bacterial pathogens. While the pathogen tries to deprive nutrients from the host cell, the host cell in return takes various metabolic countermeasures against the nutrient theft. During this conflicting interaction, the pathogen triggers metabolic host cell responses by means of common cell envelope components and specific virulence-associated factors. These host reactions generally promote replication of the pathogen. There is growing evidence that pathogen-specific factors may interfere in different ways with the complex regulatory network that controls the carbon and nitrogen metabolism of mammalian cells. The host cell defense answers include general metabolic reactions, like the generation of oxygen- and/or nitrogen-reactive species, and more specific measures aimed to prevent access to essential nutrients for the respective pathogen. Accurate results on metabolic host cell responses are often hampered by the use of cancer cell lines that already exhibit various de-regulated reactions in the primary carbon metabolism. Hence, there is an urgent need for cellular models that more closely reflect the in vivo infection conditions. The exact knowledge of the metabolic host cell responses may provide new interesting concepts for antibacterial therapies.

摘要

细菌病原体与哺乳动物宿主的相互作用导致相互作用的伙伴产生各种生理反应,旨在适应新的情况。这些反应包括受影响宿主细胞中的多种代谢变化,当病原体在宿主细胞内复制时,这些变化最为明显,就像细胞内细菌病原体一样。当病原体试图剥夺宿主细胞的营养时,宿主细胞会反过来采取各种代谢对策来抵御营养窃取。在这种相互冲突的相互作用中,病原体通过常见的细胞包膜成分和特定的与毒力相关的因子触发代谢宿主细胞反应。这些宿主反应通常促进病原体的复制。越来越多的证据表明,病原体特异性因素可能以不同的方式干扰控制哺乳动物细胞碳氮代谢的复杂调控网络。宿主细胞防御反应包括一般的代谢反应,如产生氧和/或氮反应性物质,以及更具体的措施,旨在防止进入各自病原体所需的必需营养素。由于使用已经在初级碳代谢中表现出各种失调反应的癌细胞系,因此,经常会对代谢宿主细胞反应的准确结果产生阻碍。因此,迫切需要更接近体内感染条件的细胞模型。对代谢宿主细胞反应的确切了解可能为抗菌治疗提供新的有趣概念。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c51/3705551/91e0e73ca541/fcimb-03-00024-g0001.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验