Pathogenic role of heat shock protein of Helicobacter pylori and host immune response to the heat shock protein

利用纯化的幽门螺杆菌热休克蛋白60（HSP 60）及其与β-半乳糖苷酶的融合蛋白，研究了幽门螺杆菌的热休克蛋白60与β-半乳糖苷酶的相互作用。pylori HSP 60刺激胃上皮细胞分泌白细胞介素8（IL-8），IL-8与胃粘膜炎症的诱导密切相关。此外，纯化的HSP 60可诱导胃上皮细胞凋亡。以上结果表明，H. pylori在H.在胃上皮细胞表面检测到一个与HSP 60单克隆抗体（Mab）反应的表位。对H. pylori患者血清中HSP 60表达较强。pylori感染者比无H.幽门感染HSP 60与β-半乳糖苷酶的融合蛋白以及与单克隆抗体反应的寡肽pH 9对H. pylori小鼠。提示H. pylori可能是一个很好的候选疫苗成分

By using purified heat shock protein 60 (HSP60) of Helicobacter pylori and fusion protein of HSP60 with beta-galactosidase, it was shown that H. pylori HSP60 stimulated a secretion of interleukin-8 (IL-8) which is closely related with the induction of gastric mucosal inflammation from gastric epithelial cells. In addition, purified HSP60 induced apoptosis of gastric epithelial cells. These results indicate that HSP60 of H. pylori might play an important role in pathogenesis following H. pylori infection.An epitope reactable with monoclonal antibody (Mab) to HSP60 was detected on the surface of gastric epithelial cells. Immune response to H. pylori HSP60 was stronger in the sera of the patients with H. pylori infection than in those without H. pylori infection. Not only fusion protein of HSP60 with beta-galactosidase but also oligopeptide pH9 reactable with the Mab showed a protective effect on colonization of H. pylori in mice. These results suggest that HSP60 of H. pylori might be a good candidate as a component of vaccine