Bauer Bianca, Moese Stefan, Bartfeld Sina, Meyer Thomas F, Selbach Matthias
Max-Planck-Institut für Infektionsbiologie, Abt. Molekulare Biologie, Schumannstr. 20/21, D-10117 Berlin, Germany.
Infect Immun. 2005 Aug;73(8):4643-52. doi: 10.1128/IAI.73.8.4643-4652.2005.
Helicobacter pylori persistently infects the human stomach and can cause gastritis, gastric ulceration, and gastric cancer. The type IV secretion system (TFSS) of virulent H. pylori strains translocates the CagA protein, inducing the dephosphorylation of host cell proteins and leading to changes in the morphology or shape of AGS gastric epithelial cells. Furthermore, the TFSS is involved in the induction of proinflammatory cytokines. While the H. pylori genes required for TFSS function have been investigated systematically, little is known about possible host cell factors involved. We infected 19 different mammalian cell lines individually with H. pylori and analyzed CagA translocation, dephosphorylation of host cell proteins, chemokine secretion (interleukin-8 and macrophage inflammatory protein 2), and changes in cellular phenotypes. Our results demonstrate that not only bacterial but also host cell factors determine the cellular response to infection. The identification of such unknown host cell factors will add to our understanding of host-pathogen interactions and might help in the development of new therapeutic strategies.
幽门螺杆菌持续感染人类胃部，可引发胃炎、胃溃疡和胃癌。毒力强的幽门螺杆菌菌株的IV型分泌系统（TFSS）可转运CagA蛋白，诱导宿主细胞蛋白去磷酸化，并导致AGS胃上皮细胞的形态或形状发生改变。此外，TFSS还参与促炎细胞因子的诱导。虽然已经对TFSS功能所需的幽门螺杆菌基因进行了系统研究，但对于可能涉及的宿主细胞因子却知之甚少。我们分别用幽门螺杆菌感染了19种不同的哺乳动物细胞系，并分析了CagA易位、宿主细胞蛋白去磷酸化、趋化因子分泌（白细胞介素-8和巨噬细胞炎性蛋白2）以及细胞表型的变化。我们的结果表明，不仅细菌而且宿主细胞因子也决定了细胞对感染的反应。鉴定此类未知的宿主细胞因子将增进我们对宿主-病原体相互作用的理解，并可能有助于开发新的治疗策略。
