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首页> 外文期刊>World Journal of Gastroenterology >NF-κB and ERK-signaling pathways contribute to the gene expression induced by cag PAI-positive- Helicobacter pylori infection
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NF-κB and ERK-signaling pathways contribute to the gene expression induced by cag PAI-positive- Helicobacter pylori infection

机译：NF-κB和ERK信号通路有助于cag PAI阳性幽门螺杆菌感染诱导的基因表达

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AIM: To elucidate the sequential gene expression profile in AGS cells co-cultured with wild-type Helicobacter pylori (H pylori) as a model of H pylori-infected gastric epithelium, and to further examine the contribution of cag-pathogenicity islands (cagPAI)-coding type Ⅳ secretion system and the two pathways, nuclear factor kappa B (NF-κB) and extracellular signal-regulated kinases (ERK) on wild-type H pylori-induced gene expression. METHODS: Gene expression profiles induced by H pylori were evaluated in AGS gastric epithelial cells using cDNA microarray, which were present in the 4 600 independent clones picked up from the human gastric tissue. We also analyzed the contribution of NF-κB and ERK signaling on H pylori-induced gene expression by using inhibitors of specific signal pathways. The isogenic mutant with disrupted cagE (△cagE) was used to elucidate the role of capPAI-encoding type IV secretion system in the gene expression profile. RESULTS: According to the expression profile, the genes were classified into four clusters. Among them, the clusters characterized by continuous upregulation were most conspicuous, and it contained many signal transducer activity-associated genes. The role of cagPAI on cultured cells was also investigated using isogenic mutant capE, which carries non-functional cagPAI. Then the upregulation of more than 80% of the induced genes (476/566) was found to depend on cagPAI. Signal transducer pathway through NF-κB or ERK are the major pathways which are known to be activated by cagPAI-positive H pylori. The role of these pathways in the whole signal activation by cagPAI- positive H pylori was analyzed. The specific inhibitors against NF-κB or ERK pathway blocked the activation of gene expression in 65% (367/566) or 76% (429/566) of the genes whose activation appealed to depend on cagPAI. CONCLUSION: These results suggest that more than half of the genes induced by cagPAI-positive H pylori depend on NF-κB and ERK signaling activation, and these pathways may play a role in the gene expression induced by host-bacterial interaction which may associate with H pylorirelated gastro-duodenal diseases.
机译：目的：阐明与野生型幽门螺杆菌（H pylori）共培养的AGS细胞中的顺序基因表达谱，作为幽门螺杆菌感染的胃上皮的模型，并进一步研究cag致病岛（cagPAI）的贡献编码Ⅳ型分泌系统以及核因子κB（NF-κB）和细胞外信号调节激酶（ERK）对野生型幽门螺杆菌诱导的基因表达的两个途径。方法：利用cDNA微阵列技术评估AGS胃上皮细胞中幽门螺杆菌诱导的基因表达谱，该芯片存在于从人胃组织中提取的4 600个独立克隆中。我们还通过使用特定信号途径的抑制剂分析了NF-κB和ERK信号传导对幽门螺杆菌诱导的基因表达的影响。使用具有破坏的cagE的等基因突变体（△cagE）来阐明capPAI编码的IV型分泌系统在基因表达谱中的作用。结果：根据表达谱，将基因分为四个簇。其中，以连续上调为特征的簇最为明显，并且包含许多与信号转导活性相关的基因。还使用携带无功能cagPAI的同基因突变体capE研究了cagPAI在培养细胞上的作用。然后发现超过80％的诱导基因（476/566）的上调取决于cagPAI。通过NF-κB或ERK的信号转导途径是已知的主要途径，被cagPAI阳性幽门螺杆菌激活。分析了这些途径在cagPAI阳性幽门螺杆菌完整信号激活中的作用。针对NF-κB或ERK途径的特异性抑制剂阻断了其表达依赖于cagPAI的基因的65％（367/566）或76％（429/566）中的基因表达激活。结论：这些结果表明，cagPAI阳性幽门螺杆菌诱导的基因中有一半以上依赖于NF-κB和ERK信号的激活，这些途径可能在宿主与细菌相互作用诱导的基因表达中起作用，这可能与幽门螺杆菌相关的胃十二指肠疾病。

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