蒙古沙鼠感染幽门螺杆菌后的胃部病理学变化研究

目的　建立幽门螺杆菌 (Helicobacterpylori,Hp)的蒙古沙鼠长期感染模型并观察其胃内的病理学改变。 方法　蒙古沙鼠 (8周龄 ) 80只 ,随机分为实验组 (40只 )和对照组 (40只 ) ,所有沙鼠禁食水 1d ,第 2天灌喂 5 0 %的乙醇 0 3ml,试验组第 3天及第 4天分 3次灌喂cagA Hp菌液 (10 9cfu/ml) ,0 5ml/只·次 ,对照组灌喂相同量无菌肉汤。最后一次灌喂后 2h进食水。距最后一次灌菌后 4、8、12、2 0、2 4周分别剖杀动物 ,每次实验组、对照组各 8只 ,进行微生物学检查 (粘膜涂片染色镜检、分离培养、快速尿素酶试验 )、血清学检查 (ELISA测抗Hp抗体 )和病理学检查。结果　实验组沙鼠在不同时间Hp感染率均达到 10 0 %。从第 4周开始 ,可见所有实验组沙鼠胃组织中有大量炎性细胞浸润 ,随着时间推移形成淋巴滤泡。部分沙鼠在第 12周后至 2 4周可见明显出血、慢性活动性胃炎及溃疡 ,有的溃疡可深达肌层。对照组沙鼠均无Hp定植及组织学病变。结论　蒙古沙鼠感染Hp后 ,可出现与人极相似的病理组织学改变 ,对于研究Hp的致病机制及疫苗具有重要价值

Establishment of a Mongolian gerbil model infected steadily with Helicobacter pylori

Aim To establish a chronic Mongolian gerbil model infected with Helicobacter pylori(H pylori) Methods 80 Mongolian gerbils(eight weeks old) were randomized into two groups:group 1(n=40) and group 2(n=40) After being deprived of food for 24 hours,all animals were orally fed with 0 3 ml ethanol(50%) Then,the gerbils belonging to group 1 were orally inoculated with 0 5ml broth culture of H pylori(10 9cfu/ml)by using an 18 gage feeding needle for 3 times within next 2 days,those belonging to group 2 were orally fed with sterilized broth 8 gerbils of every group were sacrificed at 4,8,12,20,24 weeks after the latest challenge and were treated for microbiological examination,serologic examination and histological examination Results From the forth week after infection,H pylori colonized steadily in the stomachs of all gerbils of group 1 and infiltration of polymorphonuclear leucocytes and mononuclear cells were observed in the lamina propria and submucosa of the stomach of the gerbils Furthermore,lymphatic follicle appeared in some animals after 8 weeks After 12 weeks,some gerbils of group 1 can be observed obviously hemorrhage,chronic active gastritis and severe ulcer in the stomach On the contrary,all the animals of group 2 were not be observed any histological change Conclusion Mongolian gerbils infected with H pylori causing ulcer and severe gastritis is one of the best animal models for studying the pathogenecity and vaccine of H pylori