Host-response in gastric mucosa in fected with Helicobacter pylori

实验结果如下：1.用沙土鼠建立十二指肠胃反流动物模型。DGR虽能降低Hp所致胃炎早期的活动性，但可加速胃上皮细胞的周转。2.A4GnT是调节腺粘液产生的关键酶。在接种Hp后的不同时间点，定量检测α4GnT、IL-1B、TNFa、IL-4、IL-6和IL-10mRNA的表达。结果：(1)幽门螺杆菌感染胃炎早期a4GnT基因表达增强。(2)IL-1B和TNFa的反应与a4GnT相同。(3)IL-4、IL-6、IL-10在幽门螺杆菌感染胃炎晚期升高。胃粘膜的免疫反应随时间变化从Th1为主到Th2为主。(4)Hp感染的胃粘膜表面形成厚厚的粘液帽。3.大米提取精华液对Hp诱导的胃炎有抑制作用。4.Hp和亚硝基化合物处理的MGs细胞因子(Th1和Th2)的表达增加。MG是研究幽门螺杆菌感染、宿主反应和环境因素之间关系的有用动物模型。

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.