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首页> 外文期刊>Biochimica et biophysica acta. Biomembranes >Delta-toxin from Clostridium perfringens perturbs intestinal epithelial barrier function in Caco-2 cell monolayers
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Delta-toxin from Clostridium perfringens perturbs intestinal epithelial barrier function in Caco-2 cell monolayers

机译：来自Cartridium的Delta-毒素Perturbs在Caco-2细胞单层中的肠道上皮阻隔功能

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Abstract Clostridium perfringens delta-toxin is a β-barrel-pore-forming toxin (β-PFT) and a presumptive virulence factor of type B and C strains, which are causative organisms of fatal intestinal diseases in animals. We showed previously that delta-toxin causes cytotoxicity via necrosis in sensitive cells. Here, we examined the effect of delta-toxin on intestinal membrane integrity. Delta-toxin led to a reduction in transepithelial electrical resistance (TEER) and increased the permeability of fluorescence isothiocyanate-conjugated dextran in human intestinal epithelial Caco-2 cells without changing the tight junction proteins, such as zonula occludens-1 (ZO-1), occludin, and claudin-1. On the other hand, delta-toxin reduced the cellular levels of adherence junction protein E-cadherin before cell injury. A disintegrin and metalloprotease (ADAM) 10 facilitates E-cadherin cleavage and was identified as the cellular receptor for alpha-toxin, a β-PFT produced by Staphylococcus aureus . ADAM10 inhibitor (GI254023X) blocked the toxin-induced decrease in TEER and cleavage of E-cadherin. Delta-toxin enhanced ADAM10 activity in a dose- and time-dependent manner. Furthermore, delta-toxin colocalized with ADAM10. These results indicated that ADAM10 plays a key role in delta-toxin-induced intestinal injury. Graphical abstract Display Omitted Highlights ? Delta-toxin impairs the barrier function of human intestinal epithelial Caco-2 cells. ? Delta-toxin induces the activation of ADAM10, and gives rise to cleavage of E-cadherin. ? Delta-toxin disrupts epithelial barrier function through the activation of ADAM10.
机译：摘要梭菌δδ-毒素是一种β-桶 - 孔形成毒素（β-PFT）和B型和C菌株的推定毒力因子，这是动物致命肠疾病的致命生物。我们以前展示δ-毒素通过敏感细胞的坏死导致细胞毒性。在这里，我们检查了δ-毒素对肠膜完整性的影响。 δ-毒素导致降低TRANSEPITHELIAL电阻（TEER），并增加人肠上皮CACO-2细胞中荧光异氰酸酯 - 缀合的葡聚糖的渗透性，而不改变紧密结蛋白，如ZONULA occludens-1（ZO-1） ，occludin和claudin-1。另一方面，δ-毒素在细胞损伤之前降低了粘附结蛋白E-钙粘蛋白的细胞水平。解毒素和金属蛋白酶（ADAM）10有助于E-Cadherin裂解，并鉴定为α-毒素的细胞受体，由金黄色葡萄球菌产生的β-PFT。 ADAM10抑制剂（GI254023x）阻断毒素诱导的毒素诱导的E-cadherin的裂解。 δ-毒素以剂量和时间依赖的方式增强了ADAM10活动。此外，δ-毒素与ADAM10结合。这些结果表明，ADAM10在δ-毒素诱导的肠损伤中起关键作用。图形抽象显示省略了亮点？ δ-毒素损害人肠上皮Caco-2细胞的阻隔功能。还δ-毒素诱导ADAM10的激活，并产生E-Cadherin的切割。还Delta-Toxin通过Adam10的激活来破坏上皮屏障功能。

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