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目的通过Ｈｐ的接种，建立沙土鼠Ｈｐ感染模型，再现同一病变，并观察除菌治疗前后炎症细胞浸润及细胞增殖的变化，研究Ｈｐ的致病过程．方法用组织化学、免疫组织化学及电镜检测病理组织学变化．结果Ｈｐ感染早期２ｗｋ以幽门粘膜为中心可见大量炎性细胞浸润，随着感染时间的增加，炎症越来越重．感染３ｍｏ后幽门部小弯附近可见溃疡出现．感染的早期以中性粒细胞浸润为主的急性炎症改变，随着感染的持续转变为以淋巴细胞浸润为主的慢性炎症改变及淋巴滤泡的广泛形成．并可见大量的肥大细胞存在，提示肥大细胞在Ｈｐ感染中起着重要作用，但作用机制不清．炎症处的ＢｒｄＵ标识率明显多于非炎症处，除菌治疗后炎症细胞及ＢｒｄＵ标识率明显减低，提示三联疗法是完全有效的消化性溃疡的治疗剂．结论Ｈｐ可感染沙土鼠导致胃炎、胃溃疡发生，其病理改变与人类类似，沙土鼠是Ｈｐ感染理想的动物模型．
Objective To establish a model of Hp infection in gerbils through inoculation of Hp, and to reproduce the same pathological changes. To observe the changes of inflammatory cell infiltration and cell proliferation before and after sterilization, and to study the pathogenic process of Hp. Methods Histochemistry, immunohistochemistry and electron microscopy were used to detect histopathological changes. Results In the early stage of Hp infection, a large number of infiltrating inflammatory cells were observed in the pyloric mucosa at 2 weeks. As the infection time increased, the inflammation became heavier and heavier. After 3mo infection of small bowel pyloric ulcers visible. The early infection with neutrophil infiltration of acute inflammatory changes, with the continuous change of infection into lymphocytic infiltration of chronic inflammatory changes and the extensive formation of lymphoid follicles. And a large number of mast cells can be seen, suggesting that mast cells play an important role in Hp infection, but the mechanism of action is unclear. Inflammation Department of BrdU labeling rate was significantly higher than the non-inflammatory, sterilization after treatment of inflammatory cells and BrdU markedly reduced the rate, suggesting triple therapy is completely effective treatment of peptic ulcer. Conclusion Hp infected gerbils lead to gastritis and gastric ulcer, and their pathological changes are similar to those in humans. Gerbils are the ideal animal model of Hp infection.