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首页> 外文期刊>Infection and immunity >Enterohemorrhagic Escherichia coli Infection Induces Interleukin-8 Production via Activation of Mitogen-Activated Protein Kinases and the Transcription Factors NF-κB and AP-1 in T84 Cells
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Enterohemorrhagic Escherichia coli Infection Induces Interleukin-8 Production via Activation of Mitogen-Activated Protein Kinases and the Transcription Factors NF-κB and AP-1 in T84 Cells

机译：肠出血性大肠杆菌感染通过激活丝裂素活化的蛋白激酶以及转录因子NF-κB和AP-1在T84细胞中诱导白介素8的产生。

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Enterohemorrhagic Escherichia coli (EHEC) infections are associated with hemorrhagic colitis and the hemolytic-uremic syndrome (HUS). In vivo, elevated plasma levels of the proinflammatory cytokine interleukin-8 (IL-8) in EHEC-infected children are correlated with a high risk of developing HUS. As IL-8 gene transcription is regulated by the transcription factors NF-κB and AP-1, we analyzed the role of these factors in the regulation of IL-8 production after infection of the epithelial intestinal T84 cell line by EHEC. By 6 h of infection, EHEC had induced significant secretion of IL-8 (35.84 ± 6.76 ng/ml versus 0.44 ± 0.04 ng/ml in control cells). EHEC induced AP-1 and NF-κB activation by 3 h of infection. Moreover, the three mitogen-activated protein kinases (MAPK) (ERK1/2, p38, and JNK) were phosphorylated in EHEC-infected T84 cells concomitant with induction of AP-1 DNA binding activity, and IκB-α was phosphorylated and then degraded concomitant with induction of NF-κB DNA binding activity. Pretreatment of cells with the highly specific MEK1/2 inhibitor U0126, the p38 inhibitor SB203580, and/or the proteasome inhibitor ALLN led to inhibition of the IL-8 secretion induced in EHEC-infected T84 cells. These findings demonstrate that (i) EHEC can induce in vitro a potent proinflammatory response by secretion of IL-8 and (ii) the secretion of IL-8 is due to the involvement of MAPK, AP-1, and NF-κB signaling pathways.
机译：肠出血性大肠埃希菌（EHEC）感染与出血性结肠炎和溶血性尿毒症综合征（HUS）有关。在体内，EHEC感染儿童的促炎细胞因子白细胞介素8（IL-8）血浆水平升高与发生HUS的高风险相关。由于IL-8基因的转录受转录因子NF-κB和AP-1的调节，因此我们分析了这些因子在EHEC感染上皮小肠T84细胞系后对IL-8产生的调节作用。感染6小时后，EHEC诱导了IL-8的显着分泌（35.84±6.76 ng / ml，而对照细胞为0.44±0.04 ng / ml）。感染3小时后，EHEC诱导AP-1和NF-κB活化。此外，三种丝裂原激活蛋白激酶（MAPK）（ERK1 / 2，p38和JNK）在感染EHEC的T84细胞中被磷酸化，同时诱导了AP-1 DNA结合活性，IκB-α被磷酸化然后降解与诱导NF-κBDNA结合活性同时发生。用高度特异性的MEK1 / 2抑制剂U0126，p38抑制剂SB203580和/或蛋白酶体抑制剂ALLN预处理细胞会导致EHEC感染的T84细胞诱导的IL-8分泌受到抑制。这些发现表明（i）EHEC可以通过分泌IL-8在体外诱导有效的促炎反应，并且（ii）IL-8的分泌归因于MAPK，AP-1和NF-κB信号通路的参与。

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