轮状病毒的NSP4肠毒素可诱导极化上皮细胞的细胞旁渗漏。
NSP4 enterotoxin of rotavirus induces paracellular leakage in polarized epithelial cells.
作者信息
Tafazoli F, Zeng C Q, Estes M K, Magnusson K E, Svensson L
机构信息
Division of Medical Microbiology, Department of Health and Environment, Linköping University, Linköping, Sweden.
出版信息
J Virol. 2001 Feb;75(3):1540-6. doi: 10.1128/JVI.75.3.1540-1546.2001.
The nonstructural NSP4 protein of rotavirus has been described as the first viral enterotoxin. In this study we have examined the effect of NSP4 on polarized epithelial cells (MDCK-1) grown on permeable filters. Apical but not basolateral administration of NSP4 was found to cause a reduction in the transepithelial electrical resistance, redistribution of filamentous actin, and an increase in paracellular passage of fluorescein isothiocyanate-dextran. Significant effects on transepithelial electrical resistance were noted after a 20- to 30-h incubation with 1 nmol of NSP4. Most surprisingly, the epithelium recovered its original integrity and electrical resistance upon removal of NSP4. Preincubation of nonconfluent MDCK-1 cells with NSP4 prevented not only development of a permeability barrier but also lateral targeting of the tight-junction-associated Zonula Occludens-1 (ZO-1) protein. Taken together, these data indicate new and specific effects of NSP4 on tight-junction biogenesis and show a novel effect of NSP4 on polarized epithelia.
轮状病毒的非结构NSP4蛋白被认为是第一种病毒肠毒素。在本研究中，我们检测了NSP4对生长在可渗透滤膜上的极化上皮细胞（MDCK-1）的影响。发现从顶端而非基底外侧给予NSP4会导致跨上皮电阻降低、丝状肌动蛋白重新分布，以及异硫氰酸荧光素-葡聚糖的细胞旁通透性增加。用1 nmol NSP4孵育20至30小时后，观察到对跨上皮电阻有显著影响。最令人惊讶的是，去除NSP4后，上皮细胞恢复了其原始完整性和电阻。用NSP4预孵育未汇合的MDCK-1细胞不仅阻止了通透性屏障的形成，还阻止了紧密连接相关的闭合蛋白1（ZO-1）蛋白的侧向定位。综上所述，这些数据表明NSP4对紧密连接生物发生有新的特异性影响，并显示了NSP4对极化上皮细胞的新作用。
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