幽门螺杆菌cag致病岛编码的蛋白质是激活核因子-κB所必需的。
Proteins encoded by the cag pathogenicity island of Helicobacter pylori are required for NF-kappaB activation.
作者信息
Glocker E, Lange C, Covacci A, Bereswill S, Kist M, Pahl H L
机构信息
Institute for Experimental Cancer Research, Tumor Biology Center, Freiburg, Germany.
出版信息
Infect Immun. 1998 May;66(5):2346-8. doi: 10.1128/IAI.66.5.2346-2348.1998.
Abstract
Helicobacter pylori is the etiological agent in the development of chronic gastritis, duodenal ulceration, and gastric adenocarcinoma. The difference in virulence between individual strains is reflected in their ability to induce interleukin-8 (IL-8) secretion from gastric epithelial cells. It has been shown that virulence is associated with the presence of a bacterial gene cluster (a pathogenicity island). We have recently demonstrated that H. pylori-mediated IL-8 secretion requires activation of the transcription factor NF-kappaB. Here, we show that NF-kappaB induction requires six membrane proteins encoded within the pathogenicity island.
摘要
幽门螺杆菌是慢性胃炎、十二指肠溃疡和胃腺癌发病的病原体。不同菌株之间的毒力差异体现在它们诱导胃上皮细胞分泌白细胞介素-8（IL-8）的能力上。研究表明，毒力与一个细菌基因簇（一个致病岛）的存在有关。我们最近证明，幽门螺杆菌介导的IL-8分泌需要转录因子NF-κB的激活。在此，我们表明NF-κB的诱导需要致病岛内编码的六种膜蛋白。
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A secreted/shed product of Helicobacter pylori activates transcription factor nuclear factor-kappa B.幽门螺杆菌的一种分泌/脱落产物可激活转录因子核因子-κB。
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cag, a pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factors.cag是幽门螺杆菌的一个致病岛，编码I型特异性和疾病相关的毒力因子。
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Heightened inflammatory response and cytokine expression in vivo to cagA+ Helicobacter pylori strains.体内对cagA+幽门螺杆菌菌株的炎症反应和细胞因子表达增强。
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