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Mechanisms and consequences of bladder cell invasion by uropathogenic Escherichia coli.尿路致病性大肠杆菌侵袭膀胱细胞的机制及后果
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本文引用的文献

1
An atomic resolution model for assembly, architecture, and function of the Dr adhesins.一种关于Dr黏附素组装、结构和功能的原子分辨率模型。
Mol Cell. 2004 Aug 27;15(4):647-57. doi: 10.1016/j.molcel.2004.08.003.
2
Interaction of Dr adhesin with collagen type IV is a critical step in Escherichia coli renal persistence.Dr黏附素与IV型胶原蛋白的相互作用是大肠杆菌在肾脏中持续存在的关键步骤。
Infect Immun. 2004 Aug;72(8):4827-35. doi: 10.1128/IAI.72.8.4827-4835.2004.
3
Zipper-like internalization of Dr-positive Escherichia coli by epithelial cells is preceded by an adhesin-induced mobilization of raft-associated molecules in the initial step of adhesion.上皮细胞对Dr阳性大肠杆菌的拉链样内化作用之前,在粘附的初始步骤中,粘附素会诱导筏相关分子的动员。
Infect Immun. 2004 Jul;72(7):3733-42. doi: 10.1128/IAI.72.7.3733-3742.2004.
4
Differential recognition of members of the carcinoembryonic antigen family by Afa/Dr adhesins of diffusely adhering Escherichia coli (Afa/Dr DAEC).弥漫性黏附大肠杆菌(Afa/Dr DAEC)的Afa/Dr黏附素对癌胚抗原家族成员的差异识别
Mol Microbiol. 2004 May;52(4):963-83. doi: 10.1111/j.1365-2958.2004.04033.x.
5
Epithelial invasion by Escherichia coli bearing Dr fimbriae is controlled by nitric oxide-regulated expression of CD55.携带Dr菌毛的大肠杆菌的上皮侵袭受一氧化氮调节的CD55表达控制。
Infect Immun. 2004 May;72(5):2907-14. doi: 10.1128/IAI.72.5.2907-2914.2004.
6
Engulfment of Neisseria gonorrhoeae: revealing distinct processes of bacterial entry by individual carcinoembryonic antigen-related cellular adhesion molecule family receptors.淋病奈瑟菌的吞噬作用:揭示癌胚抗原相关细胞粘附分子家族各受体介导细菌进入的不同过程。
Infect Immun. 2004 May;72(5):2742-52. doi: 10.1128/IAI.72.5.2742-2752.2004.
7
The uroepithelium: not just a passive barrier.尿路上皮:不仅仅是一道被动屏障。
Traffic. 2004 Mar;5(3):117-28. doi: 10.1046/j.1600-0854.2003.00156.x.
8
A toll-like receptor that prevents infection by uropathogenic bacteria.一种可预防尿路致病性细菌感染的 Toll 样受体。
Science. 2004 Mar 5;303(5663):1522-6. doi: 10.1126/science.1094351.
9
Interplay between antibacterial effectors: a macrophage antimicrobial peptide impairs intracellular Salmonella replication.抗菌效应分子之间的相互作用:一种巨噬细胞抗菌肽会损害细胞内沙门氏菌的复制。
Proc Natl Acad Sci U S A. 2004 Feb 24;101(8):2422-7. doi: 10.1073/pnas.0304455101.
10
Bacterial penetration of bladder epithelium through lipid rafts.细菌通过脂筏穿透膀胱上皮。
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尿路致病性大肠杆菌在泌尿道内的隐匿性活动。

Covert operations of uropathogenic Escherichia coli within the urinary tract.

作者信息

Bower Jean M, Eto Danelle S, Mulvey Matthew A

机构信息

Pathology Department, Division of Cell Biology and Immunology, University of Utah School of Medicine, 30 North 1900 East, Salt Lake City, Utah 84132-2501, USA.

出版信息

Traffic. 2005 Jan;6(1):18-31. doi: 10.1111/j.1600-0854.2004.00251.x.

DOI:10.1111/j.1600-0854.2004.00251.x
PMID:15569242
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2523259/
Abstract

Entry into host cells is required for many bacterial pathogens to effectively disseminate within a host, avoid immune detection and cause disease. In recent years, many ostensibly extracellular bacteria have been shown to act as opportunistic intracellular pathogens. Among these are strains of uropathogenic Escherichia coli (UPEC), the primary causative agents of urinary tract infections (UTIs). UPEC are able to transiently invade, survive and multiply within the host cells and tissues constituting the urinary tract. Invasion of host cells by UPEC is promoted independently by distinct virulence factors, including cytotoxic necrotizing factor, Afa/Dr adhesins, and type 1 pili. Here we review the diverse mechanisms and consequences of host cell invasion by UPEC, focusing also on the impact of these processes on the persistence and recurrence of UTIs.

摘要

许多细菌病原体要在宿主体内有效传播、避免被免疫系统检测到并引发疾病,就需要进入宿主细胞。近年来,许多表面上为胞外菌的细菌已被证明可作为机会性胞内病原体。其中包括尿路致病性大肠杆菌(UPEC)菌株,它是尿路感染(UTI)的主要病原体。UPEC能够在构成尿路的宿主细胞和组织内短暂侵入、存活并繁殖。UPEC对宿主细胞的侵袭由不同的毒力因子独立促进,包括细胞毒性坏死因子、Afa/Dr黏附素和1型菌毛。在此,我们综述了UPEC侵袭宿主细胞的多种机制及后果,同时也关注这些过程对UTI持续存在和复发的影响。