Helicobacter感染与胃MALT淋巴瘤的发生密切相关，而肥胖可增加其发病风险及死亡率。这两种危险因素可通过上调炎症因子IFN-γ、趋化因子CCL2以及脂肪因子leptin的表达，分别在胃组织与脂肪组织引起慢性炎症，促进肿瘤的发生。此外，肥胖与肿瘤的相关性也与髓源抑制性细胞（MDSC）有关，而在各种淋巴瘤组织中已发现MDSC的聚集。我们推测，肥胖导致的leptin高表达可能通过促进Helicobacter suis感染后IFN-γ的分泌使胃MALT形成增多。同时，CCL2的上调可能加速了MDSC的动员及其向胃黏膜的迁移，进而发挥免疫抑制效应参与胃MALT淋巴瘤的发生。本课题旨在通过对Helicobacter suis感染的肥胖小鼠的研究，来探讨以上肥胖相关的炎症和免疫调节机制在胃MALT淋巴瘤发生过程中的作用以及Helicobacter感染对肥胖时脂肪组织慢性炎症的影响。

Helicobacter infection is closely related to the tumorgenesis of gastric MALT lymphoma and obesity can increase its risk and mortality. These two risk factors induce chronic inflammation in the stomach and adipose tissue by the upregulation of inflammatory cytokines IFN-γ, chemokine CCL2 and adipokines leptin, contributing to the neoplasia. Moreover, myeloid-derived suppressor cell (MDSC) also plays a role in obesity-related tumorgenesis and its accumulation has been identified in various lymphoma tissues. We speculate that the high expression level of leptin caused by obesity can increase the formation of gastric MALT by enhancing the secretion of IFN-γ after Helicobacter suis infection. And the upregulation of CCL2 might accelerate MDSC mobilization and its migration to the gastric mucosa, enhancing the tumorgenesis of gastric MALT lymphoma via immunosuppression. In this subject, Helicobacter suis-infected obese mice model will be established to investigate the effect of obesity-induced inflammation and immune modulation on the gastric MALT lymphoma and the effect of Helicobacter infection on adipose inflammation in obesity.