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 （HSP60）和HSP60与β -半乳糖苷酶融合蛋白，发现幽门螺杆菌HSP60可刺激胃上皮细胞分泌白细胞介素-8 (IL-8)，而白细胞介素-8与胃粘膜炎症的诱导密切相关。纯化后的HSP60可诱导胃上皮细胞凋亡。提示幽门螺杆菌HSP60可能在幽门螺杆菌感染后的发病过程中起重要作用。在胃上皮细胞表面检测到HSP60单克隆抗体（Mab）可反应的表位。幽门螺杆菌感染患者血清中对HSP60的免疫反应强于未感染患者。HSP60与β -半乳糖苷酶的融合蛋白以及该单抗可获得的寡肽pH9均对小鼠幽门螺杆菌的定植具有保护作用。这些结果提示幽门螺杆菌的HSP60可能是一个很好的候选成分作为疫苗

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