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

用幽门螺杆菌TK 1402菌株（10 μ cfu/0.5ml，三次）口服感染无菌（GF）小鼠<8-9>。感染后1-9周胃粘膜持续感染幽门螺杆菌，胃粘膜部分萎缩，炎细胞浸润。提示GF小鼠是一种有效的幽门螺杆菌持续感染模型，幽门螺杆菌热休克蛋白60（HSP 60）与幽门螺杆菌对胃上皮细胞的粘附有关。用抗HSP 60单克隆抗体预处理H.pylon，可使H.pylon细胞的HSP 60数量显著减少。CF小鼠胃粘膜内有pylon定植，GF小鼠胃粘膜内注射HSP 60对胃粘膜无明显损伤。相反，口服HSP 6 O后再用幽门螺杆菌攻击，可引起胃粘膜严重的炎症变化。有趣的是，HSP 60处理组的幽门螺杆菌定殖数显著低于对照组。施用咪唑衍生物或益生菌（唾液乳杆菌、丁酸梭菌）治愈CF小鼠中的幽门螺杆菌的持续感染。这些结果表明，GF小鼠也是一个有用的模型，用于评估杀菌药物或细菌治疗幽门螺杆菌感染。

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.