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铜绿假单胞菌对铁的应答:遗传学、生物化学与毒力

The response of Pseudomonas aeruginosa to iron: genetics, biochemistry and virulence.

作者信息

Vasil M L, Ochsner U A

机构信息

Department of Microbiology, University of Colorado Health Sciences Center, Denver, CO 80262, USA.

出版信息

Mol Microbiol. 1999 Nov;34(3):399-413. doi: 10.1046/j.1365-2958.1999.01586.x.

DOI:10.1046/j.1365-2958.1999.01586.x
PMID:10564483
Abstract

During the past decade significant progress has been made towards identifying some of the schemes that Pseudomonas aeruginosa uses to obtain iron and towards cataloguing and characterizing many of the genes and gene products that are likely to play a role in these processes. This review will largely recount what we have learned in the past few years about how P. aeruginosa regulates its acquisition, intake and, to some extent, trafficking of iron, and the role of iron acquisition systems in the virulence of this remarkable opportunistic pathogen. More specifically, the genetics, biochemistry and biology of an essential regulator (Ferric uptake regulator - Fur) and a Fur-regulated alternative sigma factor (PvdS), which are central to these processes, will be discussed. These regulatory proteins directly or indirectly regulate a substantial number of other genes encoding proteins with remarkably diverse functions. These genes include: (i) other regulatory genes, (ii) genes involved in basic metabolic processes (e.g. Krebs cycle), (iii) genes required to survive oxidative stress (e.g. superoxide dismutase), (iv) genes necessary for scavenging iron (e.g. siderophores and their cognate receptors) or genes that contribute to the virulence (e.g. exotoxin A) of this opportunistic pathogen. Despite this recent expansion of knowledge about the response of P. aeruginosa to iron, many significant biological issues surrounding iron acquisition still need to be addressed. Virtually nothing is known about which of the distinct iron acquisition mechanisms P. aeruginosa brings to bear on these questions outside the laboratory, whether it be in soil, in a pipeline, on plants or in the lungs of cystic fibrosis patients.

摘要

在过去十年中,在确定铜绿假单胞菌获取铁的一些机制以及对许多可能在这些过程中发挥作用的基因和基因产物进行编目和表征方面取得了重大进展。本综述将主要讲述我们在过去几年中所了解的关于铜绿假单胞菌如何调节其铁的获取、摄取以及在一定程度上的转运,以及铁获取系统在这种重要的机会致病菌毒力中的作用。更具体地说,将讨论一种关键调节因子(铁摄取调节因子 - Fur)和一种受Fur调节的替代sigma因子(PvdS)的遗传学、生物化学和生物学,它们是这些过程的核心。这些调节蛋白直接或间接调节大量其他编码功能极其多样的蛋白质的基因。这些基因包括:(i)其他调节基因,(ii)参与基本代谢过程(如三羧酸循环)的基因,(iii)在氧化应激下生存所需的基因(如超氧化物歧化酶),(iv)清除铁所需的基因(如铁载体及其同源受体)或有助于这种机会致病菌毒力(如外毒素A)的基因。尽管最近关于铜绿假单胞菌对铁反应的知识有所扩展,但围绕铁获取的许多重要生物学问题仍有待解决。对于铜绿假单胞菌在实验室之外,无论是在土壤中、管道中、植物上还是囊性纤维化患者的肺部,会采用哪种独特的铁获取机制来应对这些问题,实际上我们几乎一无所知。

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