Induction of host signal transduction pathways by Helicobacter pylori
Induction of host signal transduction pathways by Helicobacter pylori
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DOI：
10.1073/pnas.94.14.7595
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发表时间：
1997-07-08
影响因子：
11.1
通讯作者：
Falkow, S
中科院分区：
文献类型：
--
作者：
Segal, ED;Lange, C;Falkow, S
幽门螺杆菌对培养的胃上皮细胞的粘附与几种细胞事件相关，包括145 kDa宿主蛋白的酪氨酸磷酸化;宿主细胞肌动蛋白和相关细胞蛋白的重组，如血管扩张剂刺激的磷蛋白，邻近附着的细菌细胞;以及细胞因子白细胞介素8（IL-8）的随后释放。H.从溃疡病和胃癌患者分离的幽门螺杆菌含有DNA插入，cag致病岛（派），其不存在于从无症状感染个体分离的细菌中。一些派基因的突变取消酪氨酸磷酸化和IL-8的合成，但不是细胞骨架重排。激酶抑制研究表明，有两种不同的途径在刺激IL-8从宿主细胞释放和这些H。pylori途径不依赖于酪氨酸磷酸化步骤。
Adherence of Helicobacter pylori to cultured gastric epithelial cells is associated with several cellular events, including the tyrosine phosphorylation of a 145-kDa host protein; the reorganization of the host cell actin and associated cellular proteins, like vasodilator-stimulated phosphoprotein, adjacent to the attached bacterial cell; and the subsequent release of the cytokine, interleukin 8 (IL-8). H. pylori isolated from patients with ulcer disease and gastric cancer contain a DNA insertion, the cag pathogenicity island (PAI), that is not present in bacteria isolated from individuals with asymptomatic infection. Mutations in a number of PAI genes abolish tyrosine phosphorylation and IL-8 synthesis but not the cytoskeletal rearrangements. Kinase inhibition studies suggest there are two distinct pathways operative in stimulating IL-8 release from host cells and one of these H. pylori pathways is independent of the tyrosine phosphorylation step.