Host-response in gastric mucosa in fected with Helicobacter pylori

本实验主要研究内容如下：1.建立了蒙古沙鼠十二指肠胃反流（DGR）动物模型。DGR虽然在胃炎的早期阶段降低了HP诱导的胃炎的活动性，但促进了胃上皮细胞的更新。胃内细菌植物群的改变引起胃内胃粘膜的变化。2.a4 GnT是调节胃粘膜粘液生成的关键酶。在MG中接种HP后的一些时间点定量α 4 GnT、IL-1B、TNF α、IL-4、IL-6和IL-10的mRNA表达。结果：（1）a4 GnT mRNA在HP诱导的胃炎早期表达增加。（2）IL-1B和TNF α与α 4 GnT反应相同。（3）IL-4、IL-6、IL-10在HP诱导的胃炎晚期升高。胃粘膜的免疫应答随时间由Th 1-为主向Th 2-为主变化。（4）HP感染胃粘膜表面形成厚的粘液样帽;（3）米精对HP诱导的胃炎有抑制作用;（4）HP和亚硝基化合物处理的MG中Th 1和Th 2细胞因子的表达增加。MG是研究HP感染、宿主反应和环境因素之间关系的理想动物模型。

Our experiments revealed the followings :1.The animal model of duodeno-gastric reflux (DGR) was established using Mongolian gerbils (MGs). The DGR accelerated the turnover of gastric epithelial cells, although it decreased the activity of HP-induced gastritis in the early phase of the gastritis. The alterations of bacterial flora in stomach caused the DGR.2.a4GnT is a key-enzyme to regulate the production of glandular mucous mucin. mRNA-expression of a4GnT, IL-1B, TNFa, IL-4,IL 6 and IL-10 were quantified at some points after inoculation of HP in MGs. Results : (1)mRNA-expression of a4GnT increased at early phase of HP-induced gastritis. (2)IL-1B and TNFa showed same response as a4GnT. (3)IL-4,6 and 10 increased at the late phase of HP-induced gastritis. Immune response of the gastric mucosa changed with time from Th1-to Th2-dominant. (4)Thick mucoid-caps of glandular mucous mucin were formed at mucosal surface of the stomach infected with HP.3.The extract essence of rice inhibits HP-induced gastritis.4.The expression of cytokines (both Th1 and Th2) increased in MGs that were treated with HP and nitroso-compounds. MG is a useful animal model to investigate the relationship among HP-infection, host-response and environmental factors.