幽门螺杆菌（Hp）可引起胃癌和其他消化系统疾病，但其药物耐药性越来越成为困扰治疗的难题。我们前期工作发现，维生素D在体内外都具有抗Hp作用，并且抑菌肽（CAMP）在Hp诱发小鼠慢性胃炎中发挥重要作用。因此我们提出假说，体内Vit D抗Hp作用与VitD受体（VDR）/CAMP有关。我们拟以Hp和Vit D3为处理和干预手段，以小鼠为研究对象， 探讨Hp感染后小鼠胃粘膜VDR、CAMP 和细胞因子表达的变化；VDR基因敲低小鼠Hp感染后对胃粘膜Hp定植、病理组织学以及CAMP表达的影响；1,25(OH)2D3干预对Hp感染小鼠胃粘膜病理组织学以及VDR、CAMP 和细胞因子表达影响。研究结果将对Hp根除策略提供新的思路。

Helicobacter pylori can cause gastric cancer and other digestive diseases, but the eradication treatment failure due to drug resistance baffled physicians. Our previous research showed that vitamin D had the effect of anti Hp in vitro and in vivo, and cathelicidin antimicrobial peptide (CAMP) could offset Hp induced chronic gastritis in mice. Therefore we proposed a hypothesis, Vit D anti Hp effect in vivo was related with the pathway Vit D receptor (VDR) /CAMP. Hp strain and Vit D3 were planned to use as intervention, mice as the research object, to explore the expression VDR, CAMP and proinflammatory cytokines in mouse gastric mucosa after Hp infection; the effect on Hp colonization, gastric mucosal histopathology and CAMP expression after VDR gene knockdown; the effect of 1,25 (OH)2D3 on Hp colonization, gastric mucosal histopathology as well as VDR, CAMP and cytokines expression after Hp infection. The research will provide a new strategy for Hp eradication.