Matsumoto S, Washizuka Y, Matsumoto Y, Tawara S, Ikeda F, Yokota Y, Karita M
Division of Chemotherapy, New Drug Research Laboratories, Fujisawa Pharmaceutical Co. Ltd, Osaka, Japan.
J Med Microbiol. 1997 May;46(5):391-7. doi: 10.1099/00222615-46-5-391.
Specific pathogen-free Mongolian gerbils were infected orally with Helicobacter pylori to establish a new small animal model of severe gastritis H. pylori was recovered by culture from both antrum and body over a 16-week period after a single inoculation. The number of H. pylori colonising the antrum was about 100-fold higher than in the body, and this was consistent throughout the experiment. Histological examination showed that all animals developed severe inflammation with infiltration of polymorphonuclear leucocytes and mononuclear cells into the lamina propria and submucosa of the antrum from 4 weeks after infection. From 8 weeks after infection, multifocal lymphoid follicles appeared in the lamina propria and submucosa, and micro-erosions were also observed in the epithelial layer. At 16 weeks after infection, ulceration with disruption of the lamina muscularis mucosae was observed in the antral mucosa. To determine whether H. pylori caused gastritis or not, infected gerbils were treated with amoxycillin. After the treatment, gastritis could not be seen in the gastric mucosa. Therefore, the Mongolian gerbil is a useful small animal model to study the pathogenesis of H. pylori in gastric ulceration and severe gastritis and to assess anti-H. pylori treatment.
将无特定病原体的蒙古沙鼠经口感染幽门螺杆菌，以建立一种新的严重胃炎小动物模型。单次接种后，在16周的时间里，通过培养从胃窦和胃体均分离出幽门螺杆菌。定植于胃窦的幽门螺杆菌数量比胃体中的高出约100倍，且在整个实验过程中均保持一致。组织学检查显示，从感染后4周起，所有动物均出现严重炎症，多形核白细胞和单核细胞浸润至胃窦固有层和黏膜下层。感染后8周起，固有层和黏膜下层出现多灶性淋巴滤泡，上皮层也观察到微糜烂。感染后16周，在胃窦黏膜中观察到黏膜肌层破坏的溃疡。为确定幽门螺杆菌是否导致胃炎，对感染的沙鼠用阿莫西林进行治疗。治疗后，胃黏膜中未见胃炎。因此，蒙古沙鼠是研究幽门螺杆菌在胃溃疡和严重胃炎发病机制中的作用以及评估抗幽门螺杆菌治疗的有用小动物模型。
