流行病学研究显示，H.pylori感染与炎症性肠病（IBD）的发病率呈负相关性。课题申请组前期研究显示，H.pylori感染可以诱导脾脏、肠系膜淋巴结（MLN）、胃肠黏膜中调节性B细胞（Breg）出现显著扩增。在胃部感染H.pylori后给予DSS诱导急性肠炎动物模型中，H.pylori/DSS共处理组较单纯DSS处理组小鼠肠炎表现显著减轻，且脾脏、MLN、派氏淋巴结（PPs）中Breg细胞扩增更明显。在本研究中拟通过构建H.pylori感染动物模型，检测肠道免疫状态及免疫微环境的变化，以及胃黏膜及外周淋巴组织中肠道归巢趋化因子受体的表达，研究H.pylori感染后肠黏膜免疫改变及肠道Breg细胞的增殖与来源，并通过 CD19-/-小鼠诱导DSS肠炎与Breg细胞回输实验，探索Breg细胞减轻DSS诱导肠炎的机制，为胃肠免疫对话研究奠定基础，为IBD的防治探索新的途径。

Epidemiologic studies show that there was an inverse association between Helicobacter pylori (H.pylori) and inflammatory bowel diseases (IBD). Our previous researches have shown that regulatory B cells (Bregs) in spleen,mensentric lymph nodes (MLN),gastro-intestinal mucosa expanded significantly after H.pylori infection. In the murine model of acute colitis induced by dextran sulphate sodium following H.pylori infection,H.pylori/DSS co-treated mice manifested mild colitis,and the frequencies of Bregs in spleen,MLN and PPs were higher compared with DSS treated mice. In this study, a murine model of H.pylori infection will be established to detect the changes of intestinal immunity and the immune microenvironment, as well as the expression of gut-homing chemokine receptor in gastric mucosa and secondary lymphoid tissues，with the aim of studying intestinal immunity after H.pylori infection and the expansion or sources of intestinal Bregs. We will also explore the mechanism of DSS-induced colitis alleviation caused by Bregs with a CD19-/- murine model of DSS-induced colitis and adoptive transfer of Bregs. Our study will lay the foundation of exploring the immune crosstalk between stomach and gut，provide new approach to prevention and treatment of IBD.