Collington G K, Booth I W, Donnenberg M S, Kaper J B, Knutton S
Institute of Child Health, University of Birmingham, Birmingham B4 6NH, United Kingdom.
Infect Immun. 1998 Dec;66(12):6049-53. doi: 10.1128/IAI.66.12.6049-6053.1998.
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.
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。