Segal E D, Lange C, Covacci A, Tompkins L S, Falkow S
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Proc Natl Acad Sci U S A. 1997 Jul 8;94(14):7595-9. doi: 10.1073/pnas.94.14.7595.
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.
幽门螺杆菌对培养的胃上皮细胞的黏附与多种细胞事件相关，包括一种145 kDa宿主蛋白的酪氨酸磷酸化；宿主细胞肌动蛋白及相关细胞蛋白（如血管舒张刺激磷蛋白）在附着细菌细胞附近的重组；以及随后细胞因子白细胞介素8（IL-8）的释放。从溃疡病和胃癌患者中分离出的幽门螺杆菌含有一个DNA插入片段，即cag致病岛（PAI），而从无症状感染者中分离出的细菌中不存在该片段。一些PAI基因的突变会消除酪氨酸磷酸化和IL-8合成，但不会影响细胞骨架重排。激酶抑制研究表明，在刺激宿主细胞释放IL-8方面有两条不同的途径起作用，其中幽门螺杆菌的一条途径独立于酪氨酸磷酸化步骤。
