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首页> 外文期刊>British Journal of Pharmacology >Verotoxin activates mitogen-activated protein kinase in human peripheral blood monocytes: role in apoptosis and proinflammatory cytokine release
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Verotoxin activates mitogen-activated protein kinase in human peripheral blood monocytes: role in apoptosis and proinflammatory cytokine release

机译：Verotoxin激活人外周血单核细胞中的促分裂原活化蛋白激酶：在凋亡和促炎性细胞因子释放中的作用

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1. In this study, we examined the role of mitogen-activated protein (MAP) kinases in the effects of verotoxins (VTs), from Escherichia coli O157:H7, upon both apoptosis and the release of tumour necrosis factor alpha (TNF-a) and granulocyte-macrophage colony-stimulated factor (GM-CSF) from human monocytes. 2. Both VT1 and VT2 stimulated a weak, transient increase in c-Jun-N-terminal kinase (JNK) activity and a strong activation of both p38 mitogen-activated protein kinase (MAP kinase) and extracellular-regulated kinase (ERK) activity in human monocytes, which was sustained in the case of p38 MAP kinase. 3. Stimulation of human monocytes with VT2 (100ng ml~(-1)) did not result in an increase in apoptosis; however, the toxin stimulated the release of both TNF-α and GM-CSF. 4. Pretreatment of human monocytes with the p38 MAP kinase inhibitor SB203580, at concentrations from 100nM to 10 μM, significantly decreased the VT1- and VT2-induced TNF-α and GM-CSF release from monocytes. In contrast, inhibition of MEK1 with PD98059 only significantly decreased GM-CSF release. 5. Pretrcatment of monocytes with SP600125 inhibited both GM-CSF and TNF-α production; however, significant effects upon p38 MAP kinase and ERK activation were observed. 6. Taken together, these results suggest a role for p38 MAP kinase and ERK in cytokine generation in response to the veroloxins. A role for JNK remains undetermined.
机译：1.在这项研究中，我们研究了细胞凋亡和肿瘤坏死因子α（TNF-a）释放过程中丝裂原激活蛋白（MAP）激酶在大肠杆菌O157：H7的维毒素（VT）作用中的作用。 ）和人类单核细胞的粒细胞巨噬细胞集落刺激因子（GM-CSF）。 2. VT1和VT2都刺激c-Jun-N端激酶（JNK）活性短暂而微弱的增加，并激活p38丝裂原活化蛋白激酶（MAP激酶）和细胞外调节激酶（ERK）活性在人类单核细胞中，这在p38 MAP激酶的情况下得以维持。 3.用VT2（100ng ml〜（-1））刺激人单核细胞不会导致凋亡增加。但是，毒素刺激了TNF-α和GM-CSF的释放。 4.用浓度为100nM至10μM的p38 MAP激酶抑制剂SB203580预处理人单核细胞，可显着降低VT1-和VT2诱导的TNF-α和GM-CSF从单核细胞释放。相反，用PD98059抑制MEK1仅显着降低了GM-CSF的释放。 5.用SP600125预处理单核细胞可抑制GM-CSF和TNF-α的产生；但是，观察到了对p38 MAP激酶和ERK活化的显着影响。 6.综上所述，这些结果表明p38 MAP激酶和ERK在响应veroloxins的细胞因子生成中具有作用。 JNK的角色尚未确定。

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