炎症性肠病（IBD）是最常见的消化道疾病之一，严重威胁人类健康。流行病学研究显示，幽门螺杆菌感染（Hp）与IBD发病风险呈负相关性。新近研究证实该现象只存在于CagA阳性Hp感染人群，但其机制尚不清楚。我们前期研究发现，Hp减轻小鼠结肠炎严重程度，结肠中存在Hp抗原成分，伴随结肠中2型巨噬细胞（M2）增加，M2中Nrf2、Hmox1蛋白表达升高，且结肠M2中含有Hp CagA蛋白。体外研究发现Hp依赖CagA促进M2极化，伴有Nrf2、Hmox1蛋白表达升高。由此我们推测，结肠中Hp抗原通过CagA-Nrf2-Hmox1通路促进M2极化，对慢性结肠炎发挥影响作用。本研究在前期研究基础上，拟通过体外实验和动物模型，探明慢性结肠炎中Hp通过CagA-Nrf2-Hmox1通路促进M2极化发挥抗炎作用的分子机制。此研究有助于为临床合并Hp感染的IBD患者及IBD高危因素者的合理处置提供科学依据。

Inflammatory bowel disease (IBD) is one of the most common gastrointestinal disorders, which seriously threatens human health. Large epidemiological studies and meta-analysis have demonstrated an inverse association between Helicobacter pylori (H.pylori) infection and the risk of developing IBD. Recent study has demonstrated that this phenomenon only exsits in CagA-positive H.pylori infected patients. However, the mechanisms by which H.pylori infection protects against IBD are still unclear. Our previous studies have demonstrated that H.pylori infection can alleviate the severity of colitis in mouse model while promoting the polarization of type 2 macrophages (M2) and increasing the expression of Nrf2 and Hmox1 in M2. Notably, the detection result of H.pylori antigens in colon was positive. There was H.pylori CagA protein in M2 isolated from colon. Our in-vitro study further revealed that H.pylori extracts promoted M2 polarization depending on CagA, which was accompanied by the increased expression of Nrf2 and Hmox1 in M2. Therefore, we speculate that H.pylori antigens in colon might promote M2 polarization by CagA-Nrf2-Hmox1 pathway and thus exert protective effects against IBD. On the basis of our previous study, we aim to explore the molecular mechanisms of the anti-inflammatory effect of H.pylori antigens in colon by determining whether H.pylori promote the polarization of M2 through CagA-Nrf2-Hmox1 pathway in chronic colitis with both animal models and in-vitro studies. With the increasing incidence of IBD and the widespread infection of H.pylori, it is meaningful to explore the relationship between both diseases and its underlying mechanisms, which is of great significance to clinical decision making for H.pylori infected patients with IBD and those with high risk factors for IBD.