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首页> 外文期刊>Infection and immunity >The Long-Lived Nature of Clostridium perfringens Iota Toxin in Mammalian Cells Induces Delayed Apoptosis
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The Long-Lived Nature of Clostridium perfringens Iota Toxin in Mammalian Cells Induces Delayed Apoptosis

机译：产气荚膜梭状芽孢杆菌Iota毒素在哺乳动物细胞中的长寿命性质诱导延迟凋亡。

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Mono-ADP ribosylation of actin by bacterial toxins, such as Clostridium perfringens iota or Clostridium botulinum C2 toxins, results in rapid depolymerization of actin filaments and cell rounding. Here we report that treatment of African green monkey kidney (Vero) cells with iota toxin resulted in delayed caspase-dependent death. Unmodified actin did not reappear in toxin-treated cells, and enzyme-active toxin was detectable in the cytosol for at least 24 h. C2 toxin showed comparable, long-lived effects in cells, while a C2 toxin control lacking ADP-ribosyltransferase activity did not induce cell death. To address whether the remarkable stability of the iota and C2 toxins in cytosol was crucial for inducing cell death, we treated cells with C/SpvB, the catalytic domain of Salmonella enterica SpvB. Although C/SpvB also mono-ADP ribosylates actin as do the iota and C2 toxins, cells treated with a cell-permeating C/SpvB fusion toxin became rounded but recovered and remained viable. Moreover, unmodified actin reappeared in these cells, and ADP-ribosyltransferase activity due to C/SpvB was not detectable in the cytosol after 24 h, a result most likely due to degradation of C/SpvB. Repeated application of C/SpvB prevented recovery of cells and reappearance of unmodified actin. In conclusion, a complete but transient ADP ribosylation of actin was not sufficient to trigger apoptosis, implying that long-term stability of actin-ADP-ribosylating toxins, such as iota and C2, in the cytosol is crucial for inducing delayed, caspase-dependent cell death.
机译：细菌毒素，例如产气荚膜梭状芽孢杆菌或肉毒梭状芽孢杆菌C2毒素，对肌动蛋白进行单ADP核糖基化，导致肌动蛋白丝迅速解聚和细胞变圆。在这里，我们报告说，使用Iota毒素治疗非洲绿猴肾脏（Vero）细胞会导致caspase依赖性死亡延迟。未修饰的肌动蛋白未在毒素处理过的细胞中重新出现，并且在细胞溶质中至少24小时可检测到酶活性毒素。 C2毒素在细胞中显示出可比的长期作用，而缺乏ADP-核糖基转移酶活性的C2毒素对照则不会诱导细胞死亡。为了解决细胞溶质中iota和C2毒素的显着稳定性是否对诱导细胞死亡至关重要，我们用C / SpvB（肠炎沙门氏菌 SpvB的催化域）处理了细胞。尽管C / SpvB也像iota和C2毒素一样，单ADP核糖基化作用肌动蛋白，但用渗透细胞的C / SpvB融合毒素处理的细胞却变圆了，但仍恢复了活力。此外，未修饰的肌动蛋白重新出现在这些细胞中，并且由于C / SpvB而导致的ADP-核糖基转移酶活性在24小时后仍未在细胞质中检测到，其结果很可能是C / SpvB的降解。重复使用C / SpvB阻止了细胞的恢复和未修饰肌动蛋白的重新出现。总之，肌动蛋白的完整但短暂的ADP核糖基化不足以引发细胞凋亡，这表明肌醇中肌动蛋白-ADP-核糖基化毒素（如iota和C2）的长期稳定性对于诱导延迟的caspase依赖性至关重要细胞死亡。

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