Study on pathogenecity of Helicobacter pylori in gastroduodenum using germ-free mice.

无菌小鼠经口感染幽门螺杆菌TK1402菌株（10^<8-9> cfu/ 0.5 ml， 3次）。感染后1 ~ 9周，小鼠胃黏膜持续感染幽门螺旋杆菌，可见炎性细胞浸润，胃黏膜部分萎缩。这些结果表明GF小鼠是持久幽门螺旋杆菌感染的有效模型。H.pylon的热休克蛋白60 （hsp60）与H.pylon对胃上皮细胞的粘附有关。用抗hsp60单克隆抗体预处理幽门螺杆菌，可显著减少幽门螺杆菌在CF小鼠胃黏膜中的定植数量。胃粘膜注射hsp60对GF小鼠胃无明显损伤。相比之下，口服hsp60后刺激幽门螺旋杆菌可引起胃黏膜严重的炎症变化。有趣的是，用hsp60处理后，H.pylon的定殖数量明显低于对照组。给予咪唑衍生物或益生菌（唾液乳杆菌、丁酸梭菌）治疗CF小鼠持续性幽门螺旋杆菌感染。这些结果表明GF小鼠也可作为评价幽门螺旋杆菌感染的杀菌药物或细菌治疗的有效模型。

Germ-free (GF) mouse was orally infected with Helicobacter pylon TK1402 strain (10^<8-9> cfu/ 0.5 ml, three times). Persistent infection of H.pylon in gastric mucosa of the mouse was demonstrated from 1-9 weeks after the infection, and infiltration of inflammatory cells and partial atrophy of gastric mucosa was detected. These results indicate that GF mouse is a useful model for persistent H.pylon infection.Heat shock protein 60 (HSP6O) of H.pylon was shown to be associated with adhesion of H.pylon to gastric epithelial cells. Pretreatment of H.pylon with anti-HSP6O monoclonal antibody resulted in a significant decrease of the number of h. pylon colonized in gastric mucosa of CF mouse.Administration of HSP6O into gastric mucosa of GF mouse induced no significant gastric damage. In contrast, oral administration of HSP6O followed by challenge of H.pylon induced severe inflammatory change in the gastric mucosa. Interestingly, the number of H.pylon colonized was significantly lower by adminstration of HSP6O than that of control. Administration of imidazole derivatives or probiotics (Lactobacillus salivanius, Clostnidium butynicum) cured the persistent infection with H.pylon in CF mouse. These results indicate that GF mouse is also a useful model for evaluation of bactericidal drug or bacteriotherapy for H.pylon infection.