Singh Anand Prakash, Aijaz Saima
Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi, 110067, India.
F1000Res. 2015 Jul 13;4:231. doi: 10.12688/f1000research.6778.2. eCollection 2015.
Enteropathogenic E. coli (EPEC) causes acute intestinal infections in infants in the developing world. Infection typically spreads through contaminated food and water and leads to severe, watery diarrhea. EPEC attaches to the intestinal epithelial cells and directly injects virulence factors which modulate multiple signaling pathways leading to host cell dysfunction. However, the molecular mechanisms that regulate the onset of diarrhea are poorly defined. A major target of EPEC is the host cell tight junction complex which acts as a barrier and regulates the passage of water and solutes through the paracellular space. In this review, we focus on the EPEC effectors that target the epithelial barrier, alter its functions and contribute to leakage through the tight junctions.
肠致病性大肠杆菌(EPEC)在发展中世界导致婴儿急性肠道感染。感染通常通过受污染的食物和水传播,并导致严重的水样腹泻。EPEC附着于肠道上皮细胞,并直接注入毒力因子,这些因子调节多种信号通路,导致宿主细胞功能障碍。然而,调节腹泻发作的分子机制尚不清楚。EPEC的一个主要靶点是宿主细胞紧密连接复合体,它作为一道屏障,调节水和溶质通过细胞旁间隙的通道。在这篇综述中,我们重点关注靶向上皮屏障、改变其功能并导致通过紧密连接渗漏的EPEC效应蛋白。