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鼠伤寒沙门氏菌血清型 Typhimurium 和 Typhi 作为模式生物:揭示宿主-病原体相互作用的范例。

Salmonella enterica serovars Typhimurium and Typhi as model organisms: revealing paradigm of host-pathogen interactions.

机构信息

Department of Microbiology and Cell Biology, Centre for Infectious Disease Research and Biosafety Laboratories, Indian Institute of Science, Bangalore, India.

出版信息

Virulence. 2012 Jul 1;3(4):377-88. doi: 10.4161/viru.21087. Epub 2012 Jun 22.

DOI:10.4161/viru.21087
PMID:22722237
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3478240/
Abstract

The lifestyle of intracellular pathogens has always questioned the skill of a microbiologist in the context of finding the permanent cure to the diseases caused by them. The best tool utilized by these pathogens is their ability to reside inside the host cell, which enables them to easily bypass the humoral immunity of the host, such as the complement system. They further escape from the intracellular immunity, such as lysosome and inflammasome, mostly by forming a protective vacuole-bound niche derived from the host itself. Some of the most dreadful diseases are caused by these vacuolar pathogens, for example, tuberculosis by Mycobacterium or typhoid fever by Salmonella. To deal with such successful pathogens therapeutically, the knowledge of a host-pathogen interaction system becomes primarily essential, which further depends on the use of a model system. A well characterized pathogen, namely Salmonella, suits the role of a model for this purpose, which can infect a wide array of hosts causing a variety of diseases. This review focuses on various such aspects of research on Salmonella which are useful for studying the pathogenesis of other intracellular pathogens.

摘要

胞内病原体的生活方式一直对微生物学家在寻找治疗由它们引起的疾病的永久方法方面的技能提出了质疑。这些病原体利用的最佳工具是它们能够存在于宿主细胞内的能力,这使它们能够轻易地绕过宿主的体液免疫,如补体系统。它们还通过形成源自宿主自身的保护性囊泡结合龛来逃避细胞内免疫,如溶酶体和炎症小体。一些最可怕的疾病是由这些囊泡病原体引起的,例如结核分枝杆菌引起的结核病或伤寒沙门氏菌引起的伤寒。为了在治疗上应对这些成功的病原体,宿主-病原体相互作用系统的知识就变得至关重要,而这进一步取决于模型系统的使用。一种具有良好特征的病原体,即沙门氏菌,适合为此目的充当模型,它可以感染广泛的宿主,引起多种疾病。本综述重点介绍了沙门氏菌的各种研究方面,这些方面对于研究其他胞内病原体的发病机制很有用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d477/3478240/e878b3c8c8e1/viru-3-377-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d477/3478240/5780de7bdb22/viru-3-377-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d477/3478240/7c9474b9fdb1/viru-3-377-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d477/3478240/e878b3c8c8e1/viru-3-377-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d477/3478240/5780de7bdb22/viru-3-377-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d477/3478240/7c9474b9fdb1/viru-3-377-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d477/3478240/e878b3c8c8e1/viru-3-377-g3.jpg

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Early immune dynamics following infection with Salmonella enterica serovars Enteritidis, Infantis, Pullorum and Gallinarum: cytokine and chemokine gene expression profile and cellular changes of chicken cecal tonsils.感染肠炎沙门氏菌血清型肠炎、婴儿、鸡白痢和鸡伤寒后的早期免疫动态:鸡盲肠扁桃体的细胞因子和趋化因子基因表达谱和细胞变化。
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induced SIRT1 and SIRT3 are crucial for maintaining the metabolic switch in bacteria and host for successful pathogenesis.诱导产生的SIRT1和SIRT3对于维持细菌和宿主中的代谢转换以实现成功致病至关重要。
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NLRP6 induces RIP1 kinase-dependent necroptosis via TAK1-mediated p38/MK2 phosphorylation in . infection.在感染过程中,NLRP6通过TAK1介导的p38/MK2磷酸化诱导RIP1激酶依赖性坏死性凋亡。
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Dynamics of macrophage polarization support persistence in a whole living organism.巨噬细胞极化的动力学支持在整个生物体中的持续存在。
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Pathogenic bacteria experience pervasive RNA polymerase backtracking during infection.在感染过程中,病原细菌会经历普遍的 RNA 聚合酶回溯。
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Pathogenic bacteria experience pervasive RNA polymerase backtracking during infection.病原菌在感染过程中普遍存在RNA聚合酶回溯现象。
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