Helicobacter pylori (H. pylori) infection is closely associated with the occurrence and development of gastric diseases. Therefore, eliminating H. pylori infection should help to prevent gastric diseases. Vitamin D3 (VitD3, 1,25(OH)₂D₃) was previously observed to exhibit anti-H. pylori infection activity in clinic, but these results were reported in heterogeneous in vivo studies without elucidation of the underlying mechanisms. In the present study, we established H. pylori infection models in both wild-type and VDR knockdown (VDR^-KD) mice, which were used to demonstrate that VitD3 inhibits H. pylori infection by enhancing the expression of VitD receptor (VDR) and cathelicidin antimicrobial peptide (CAMP). Furthermore, VDR^-KD mice that exhibited lower VDR expression were more susceptible to H. pylori infection. In cultured mouse primary gastric epithelial cells, we further demonstrated that the VitD3/VDR complex binds to the CAMP promoter region to increase its expression. These data provide a mechanistic explanation of the anti-H. pylori infection activity of VitD3 at the molecular level in mice and suggest a new avenue for the clinical management of H. pylori eradication therapy.

幽门螺杆菌（H. pylori）感染与胃部疾病的发生、发展密切相关。因此，消除幽门螺杆菌感染应该有助于预防胃部疾病。此前观察到维生素 D3 (VitD3, 1,25(OH) ₂ D ₃ ) 具有抗 H.幽门螺杆菌感染在临床上的活动，但这些结果是在异质的体内研究中报告的，而没有阐明潜在的机制。在本研究中，我们在野生型和VDR敲低（VDR ^-KD ）小鼠中建立了幽门螺杆菌感染模型，用于证明VitD3通过增强VitD受体（VDR）的表达来抑制幽门螺杆菌感染，并抑制幽门螺杆菌感染。抗菌素抗菌肽（CAMP）。此外，表现出较低VDR表达的VDR ^-KD小鼠更容易受到幽门螺杆菌感染。在培养的小鼠原代胃上皮细胞中，我们进一步证明 VitD3/VDR 复合物与 CAMP 启动子区域结合以增加其表达。这些数据提供了抗 H. VitD3 在小鼠体内分子水平上的幽门螺杆菌感染活性，为幽门螺杆菌根除治疗的临床管理提供了一条新途径。