Collington G K, Booth I W, Knutton S
Institute of Child Health, University of Birmingham, UK.
Gut. 1998 Feb;42(2):200-7. doi: 10.1136/gut.42.2.200.
The pathophysiology of enteropathogenic Escherichia coli (EPEC) diarrhoea remains uncertain. EPEC adhere to enterocytes and transduce signals which produce a characteristic "attaching and effacing" (A/E) lesion in the brush border membrane. The present in vitro study was designed to determine whether signal transduction by EPEC also influences electrolyte transport.
Caco-2 cell monolayers were rapidly infected with wild type EPEC strain E2348/69, or the signal transduction-defective mutant 14.2.1(1), and mounted in Ussing chambers.
Strain E2348/69 stimulated a rapid but transient increase in short circuit current (Isc) which coincided with A/E lesion formation; this Isc response was absent on infection with strain 14.2.1(1). While the initial rise in Isc induced by E2348/69 was partially (approximately 35%) dependent on chloride, the remainder possibly represents an influx of sodium and amino acid(s) across the apical membrane.
The study directly shows that, after initial adhesion, EPEC induce major alterations in host cell electrolyte transport. The observed Isc responses indicate a rapid modulation of electrolyte transport in Caco-2 cells by EPEC, including stimulation of chloride secretion, for which signal transduction to host cells is a prerequisite.
肠致病性大肠杆菌（EPEC）腹泻的病理生理学仍不明确。EPEC黏附于肠上皮细胞并传导信号，从而在刷状缘膜上产生特征性的“黏附与抹除”（A/E）损伤。本体外研究旨在确定EPEC的信号传导是否也会影响电解质转运。
用野生型EPEC菌株E2348/69或信号传导缺陷型突变体14.2.1(1)快速感染Caco-2细胞单层，并将其置于尤斯灌流小室中。
菌株E2348/69刺激短路电流（Isc）迅速但短暂增加，这与A/E损伤形成同时发生；感染菌株14.2.1(1)时未出现这种Isc反应。虽然E2348/69诱导的Isc初始升高部分（约35%）依赖于氯离子，但其余部分可能代表钠和氨基酸通过顶端膜的内流。
该研究直接表明，在初始黏附后，EPEC会引起宿主细胞电解质转运的重大改变。观察到的Isc反应表明EPEC可快速调节Caco-2细胞中的电解质转运，包括刺激氯离子分泌，而向宿主细胞的信号传导是其前提条件。
