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首页> 外文期刊>Infection and immunity >Shiga Toxins 1 and 2 Translocate Differently across Polarized Intestinal Epithelial Cells
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Shiga Toxins 1 and 2 Translocate Differently across Polarized Intestinal Epithelial Cells

机译：志贺毒素1和2在极化肠道上皮细胞中的转运不同

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Shiga toxin-producing Escherichia coli (STEC) is an important food-borne pathogen that causes hemolytic-uremic syndrome. Following ingestion, STEC cells colonize the intestine and produce Shiga toxins (Stx), which appear to translocate across the intestinal epithelium and subsequently reach sensitive endothelial cell beds. STEC cells produce one or both of two major toxins, Stx1 and Stx2. Stx2-producing STEC is more often associated with disease for reasons as yet undetermined. In this study, we used polarized intestinal epithelial cells grown on permeable filters as a model to compare Stx1 and Stx2 movement across the intestinal epithelium. We have previously shown that biologically active Stx1 is able to translocate across cell monolayers in an energy-dependent, saturable manner. This study demonstrates that biologically active Stx2 is also capable of movement across the epithelium without affecting barrier function, but significantly less Stx2 crossed monolayers than Stx1. Chilling the monolayers to 4°C reduced the amount of Stx1 and Stx2 movement by 200-fold and 20-fold respectively. Stx1 movement was clearly directional, favoring an apical-to-basolateral translocation, whereas Stx2 movement was not. Colchicine reduced Stx1, but not Stx2, translocation. Monensin reduced the translocation of both toxins, but the effect was more pronounced with Stx1. Brefeldin A had no effect on either toxin. Excess unlabeled Stx1 blocks the movement of125I-Stx1. Excess Stx2 failed to have any effect on Stx1 movement. Our data suggests that, despite the many common physical and biochemical properties of the two toxins, they appear to be crossing the epithelial cell barrier by different pathways.
机译：产生志贺毒素的大肠杆菌（STEC）是一种重要的食源性病原体，可引起溶血性尿毒症综合征。摄入后，STEC细胞在肠道内定殖并产生志贺毒素（Stx），似乎在肠道上皮中移位并随后到达敏感的内皮细胞床。 STEC细胞产生两种主要毒素中的一种或两种，即Stx1和Stx2。由于尚未确定的原因，产生Stx2的STEC通常与疾病相关。在这项研究中，我们使用在渗透性滤膜上生长的极化肠上皮细胞作为模型，比较了Stx1和Stx2在整个肠上皮中的运动。我们以前已经表明，具有生物活性的Stx1能够以能量依赖，可饱和的方式跨细胞单层转运。这项研究表明，具有生物活性的Stx2也能够在不影响屏障功能的情况下跨上皮移动，但与Stx1相比，Stx2交叉的单层膜明显更少。将单层冷却至4°C可使Stx1和Stx2移动量分别减少200倍和20倍。 Stx1运动显然是方向性的，有利于心尖到基底外侧移位，而Stx2运动则不是。秋水仙碱减少了Stx1的转运，但没有减少Stx2的转运。莫能菌素减少了两种毒素的转运，但Stx1的作用更为明显。布雷菲德菌素A对任何一种毒素都没有作用。过量的未标记Stx1阻止了 125 I-Stx1的移动。多余的Stx2对Stx1的移动没有​​任何影响。我们的数据表明，尽管两种毒素具有许多共同的物理和生化特性，但它们似乎通过不同的途径穿越上皮细胞屏障。

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