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编码分泌信号蛋白的肠致病性大肠杆菌毒力基因对于调节Caco-2细胞电解质转运至关重要。

Enteropathogenic Escherichia coli virulence genes encoding secreted signalling proteins are essential for modulation of Caco-2 cell electrolyte transport.

作者信息

Collington G K, Booth I W, Donnenberg M S, Kaper J B, Knutton S

机构信息

Institute of Child Health, University of Birmingham, Birmingham B4 6NH, United Kingdom.

出版信息

Infect Immun. 1998 Dec;66(12):6049-53. doi: 10.1128/IAI.66.12.6049-6053.1998.

DOI:10.1128/IAI.66.12.6049-6053.1998
PMID:9826396
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC108772/
Abstract

The pathophysiology of enteropathogenic Escherichia coli (EPEC) diarrhea remains uncertain. In vitro, EPEC stimulates a rapid increase in short-circuit current (Isc) across Caco-2 cell monolayers coincident with intimate attaching and effacing (A/E) bacterial adhesion. This study has examined the roles of specific EPEC virulence proteins in this Isc response. EPEC genes encoding EspA, EspB, and EspD, essential for signal transduction in host cells and A/E activity, were also required for modulation of Caco-2 electrolyte transport.

摘要

肠致病性大肠杆菌（EPEC）腹泻的病理生理学仍不明确。在体外，EPEC刺激跨Caco-2细胞单层的短路电流（Isc）迅速增加，同时伴有紧密黏附和消除（A/E）细菌黏附。本研究检测了特定EPEC毒力蛋白在这种Isc反应中的作用。编码EspA、EspB和EspD的EPEC基因是宿主细胞信号转导和A/E活性所必需的，也是调节Caco-2电解质转运所必需的。

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Enteropathogenic Escherichia coli virulence genes encoding secreted signalling proteins are essential for modulation of Caco-2 cell electrolyte transport.编码分泌信号蛋白的肠致病性大肠杆菌毒力基因对于调节Caco-2细胞电解质转运至关重要。
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本文引用的文献

1
The complete sequence of the locus of enterocyte effacement (LEE) from enteropathogenic Escherichia coli E2348/69.肠致病性大肠杆菌E2348/69的肠细胞脱落位点（LEE）的完整序列。
Mol Microbiol. 1998 Apr;28(1):1-4. doi: 10.1046/j.1365-2958.1998.00783.x.
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A novel EspA-associated surface organelle of enteropathogenic Escherichia coli involved in protein translocation into epithelial cells.一种与肠致病性大肠杆菌 EspA 相关的新型表面细胞器，参与蛋白质转运至上皮细胞。
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Rapid modulation of electrolyte transport in Caco-2 cell monolayers by enteropathogenic Escherichia coli (EPEC) infection.肠致病性大肠杆菌（EPEC）感染对Caco-2细胞单层中电解质转运的快速调节作用。
Gut. 1998 Feb;42(2):200-7. doi: 10.1136/gut.42.2.200.
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Enteropathogenic E. coli (EPEC) transfers its receptor for intimate adherence into mammalian cells.肠道致病性大肠杆菌（EPEC）将其紧密黏附受体转移至哺乳动物细胞中。
Cell. 1997 Nov 14;91(4):511-20. doi: 10.1016/s0092-8674(00)80437-7.
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Enteropathogenic Escherichia coli protein secretion is induced in response to conditions similar to those in the gastrointestinal tract.肠道致病性大肠杆菌的蛋白质分泌是在类似于胃肠道环境的条件下被诱导产生的。
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Intimin-dependent binding of enteropathogenic Escherichia coli to host cells triggers novel signaling events, including tyrosine phosphorylation of phospholipase C-gamma1.肠道致病性大肠杆菌对宿主细胞的紧密素依赖性结合引发了新的信号转导事件，包括磷脂酶C-γ1的酪氨酸磷酸化。
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A third secreted protein that is encoded by the enteropathogenic Escherichia coli pathogenicity island is required for transduction of signals and for attaching and effacing activities in host cells.肠道致病性大肠杆菌致病岛编码的第三种分泌蛋白是宿主细胞信号转导以及紧密黏附与抹平活性所必需的。
Infect Immun. 1997 Jun;65(6):2211-7. doi: 10.1128/iai.65.6.2211-2217.1997.
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Type III secretion systems: machines to deliver bacterial proteins into eukaryotic cells?III型分泌系统：将细菌蛋白输送到真核细胞中的机器？
Trends Microbiol. 1997 Apr;5(4):148-56. doi: 10.1016/S0966-842X(97)01029-9.
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Infection of T84 cells with enteropathogenic Escherichia coli alters barrier and transport functions.用肠致病性大肠杆菌感染T84细胞会改变屏障和转运功能。
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Enteropathogenic Escherichia coli markedly decreases the resting membrane potential of Caco-2 and HeLa human epithelial cells.肠道致病性大肠杆菌显著降低Caco-2和HeLa人上皮细胞的静息膜电位。
Infect Immun. 1996 Nov;64(11):4820-5. doi: 10.1128/iai.64.11.4820-4825.1996.