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首页> 外文期刊>Infection and immunity >Helicobacter pylori Induces RANTES through Activation of NF-κB
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Helicobacter pylori Induces RANTES through Activation of NF-κB

机译：幽门螺杆菌通过激活NF-κB诱导RANTES

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Helicobacter pylori-infected gastric mucosa displays a conspicuous infiltration of mononuclear cells and neutrophils. RANTES (short for “regulated upon activation, normal T cell expressed and secreted”) is a chemoattractant cytokine (chemokine) important in the infiltration of T lymphocytes and monocytes. RANTES may therefore contribute to the cellular infiltrate in the H. pylori-infected gastric mucosa. The aim of this study was to analyze the molecular mechanism responsible for H. pylori-mediated RANTES expression. We observed that gastric epithelial cells produced RANTES upon coculture with H. pylori. In addition, H. pylori induced RANTES mRNA expression and an increase in luciferase activity in cells which were transfected with a luciferase reporter construct derived from the RANTES promoter, in gastric epithelial cells, indicating that the induction of RANTES production occurred at the transcriptional level. Induction of RANTES was dependent on an intact cag pathogenicity island. Activation of the RANTES promoter by H. pylori occurred through the action of NF-κB. Transfection of kinase-deficient mutants of IκB kinase (IKK) and NF-κB-inducing kinase (NIK) inhibited H. pylori-mediated RANTES activation. In contrast, tumor necrosis factor alpha- or interleukin-1/Toll-like receptor signaling molecules—such as mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1, MyD88, and interleukin-1 receptor-associated kinase—did not play a role in RANTES activation by H. pylori. Collectively, H. pylori induced NF-κB activation through an intracellular signaling pathway that involved IKK and NIK, leading to RANTES gene transcription. RANTES induction by H. pylori may play an important role in gastric inflammation.
机译：幽门螺杆菌感染的胃粘膜表现出明显的单核细胞和中性粒细胞浸润。 RANTES（“激活后调节，正常T细胞表达和分泌”的缩写）是一种化学吸引细胞因子（趋化因子），在T淋巴细胞和单核细胞的浸润中很重要。因此，RANTES可能有助于细胞在 H中的浸润。幽门螺杆菌感染的胃粘膜这项研究的目的是分析造成 H的分子机制。幽门螺杆菌介导的RANTES表达我们观察到胃上皮细胞与 H共培养后产生RANTES。幽门炎。此外， H。幽门螺杆菌在胃上皮细胞中诱导了RANTES mRNA的表达，并被RANTES启动子衍生的萤光素酶报告基因构建体转染的细胞中的萤光素酶活性增加，表明RANTES产生的诱导发生在转录水平。 RANTES的诱导取决于完整的 cag 致病岛。 EM激活RANTES启动子。幽门螺杆菌是通过NF-κB的作用而发生的。 IκB激酶（IKK）和NF-κB诱导激酶（NIK）的激酶缺陷型突变体的转染抑制了 H。幽门螺杆菌介导的RANTES激活相反，肿瘤坏死因子α或白介素-1 / Toll样受体信号分子（如促分裂原激活蛋白激酶/细胞外信号调节激酶激酶1，MyD88和白介素-1受体相关激酶）没有发挥作用在 H激活RANTES中发挥作用。幽门炎。统称为 H。幽门螺杆菌通过涉及IKK和NIK的细胞内信号通路诱导NF-κB活化，导致RANTES基因转录。通过 H进行RANTES诱导。幽门螺杆菌在胃炎中可能起重要作用。

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