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首页> 外文期刊>Infection and immunity >The Enteropathogenic Escherichia coli Effector Cif Induces Delayed Apoptosis in Epithelial Cells
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The Enteropathogenic Escherichia coli Effector Cif Induces Delayed Apoptosis in Epithelial Cells

机译：肠致病性大肠杆菌效应因子CIF诱导上皮细胞延迟凋亡。

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The cycle inhibiting factor (Cif) belongs to a family of bacterial toxins, the cyclomodulins, which modulate the host cell cycle. Upon injection into the host cell by the type III secretion system of enteropathogenic Escherichia coli (EPEC), Cif induces both G2 and G1 cell cycle arrests. The cell cycle arrests correlate with the accumulation of p21waf1 and p27kip1 proteins that inhibit CDK-cyclin complexes, whose activation is required for G1/S and G2/M transitions. Increases of p21 and p27 levels are independent of p53 transcriptional induction and result from protein stabilization through inhibition of the ubiquitin/proteasome degradation pathway. In this study, we show that Cif not only induces cell cycle arrest but also eventually provokes a delayed cell death. Indeed, 48 h after infection with EPEC expressing Cif, cultured IEC-6 intestinal cells were positive for extracellular binding of annexin V and exhibited high levels of cleaved caspase-3 and lactate dehydrogenase release, indicating evidence of apoptosis. Cif was necessary and sufficient for inducing this late apoptosis, and the cysteine residue of the catalytic site was required for Cif activity. These results highlight a more complex role of Cif than previously thought, as a cyclomodulin but also as an apoptosis inducer.
机译：周期抑制因子（Cif）属于细菌毒素家族，即调节宿主细胞周期的环调节蛋白。通过肠致病性大肠埃希氏菌（EPEC）的III型分泌系统注入宿主细胞后，Cif诱导G 2 和G 1 细胞循环逮捕。细胞周期停滞与抑制CDK细胞周期蛋白复合物的p21 waf1 和p27 kip1 蛋白的积累有关，后者激活G 1 是必需的。 / S和G 2 / M转换。 p21和p27水平的增加与p53转录诱导无关，并且是通过抑制遍在蛋白/蛋白酶体降解途径来稳定蛋白质而导致的。在这项研究中，我们显示Cif不仅诱导细胞周期停滞，而且最终引起延迟的细胞死亡。确实，在感染表达EPEC的Cif后48小时，培养的IEC-6肠细胞对膜联蛋白V的胞外结合呈阳性，并表现出高水平的caspase-3裂解和乳酸脱氢酶释放，表明有凋亡迹象。 Cif对于诱导该晚期细胞凋亡是必要和充分的，并且Cif活性需要催化位点的半胱氨酸残基。这些结果突显了Cif作为环调节蛋白，同时还作为凋亡诱导因子，其作用比以前认为的更为复杂。

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