Zhang Ye, Wang Chunya, Zhang Li, Yu Jie, Yuan Wenjie, Li Lei
Department of Gastroenterology, Affiliated Hospital of Weifang Medical University, Weifang, China.
Department of Hepatobiliary Surgery, The First Affiliated Hospital, Kunming Medical University, Kunming, China.
Front Microbiol. 2022 Dec 8;13:1033201. doi: 10.3389/fmicb.2022.1033201. eCollection 2022.
Vitamin D [VitD, 1,25 (OH)D] is known to have immunomodulatory and anti-microbial properties; however, its activity against is unclear. In this study, we established infection models in wild-type and VitD receptor (VDR) knockdown mice and analyzed the effects of VitD and their underlying mechanisms.
VDR and VDR mice were intragastrically infected with the SS1 strain. After confirmation of infection, mice were treated with different doses of VitD. The infection levels in stomach tissues were quantified using the colony-forming assay, and the expression levels of the VDR and cathelicidin antimicrobial peptide (CAMP) in the gastric mucosa were analyzed by immunohistochemistry and western blotting.
The gastric mucosa of VDR mice was more susceptible to colonization and had lower levels of VDR and CAMP expression than that of VDR mice. infection upregulated VDR and CAMP expression in the stomach of both wild-type and mutant mice, and VitD treatment resulted in further increase of VDR and CAMP levels, while significantly and dose-dependently decreasing the colonization rate in both mouse groups, without affecting blood calcium or phosphorus levels.
Our data indicate that oral administration of VitD reduces the colonization rate and upregulates VDR and CAMP expression in the gastric mucosa, suggesting a role for VitD/VDR/CAMP signaling in the eradication of in the stomach. These findings provide important insights into the mechanism underlying the anti- activity of VitD and should be useful in the development of measures to eradicate .
维生素D [VitD，1,25 (OH)D] 具有免疫调节和抗菌特性；然而，其对[具体病菌未提及]的活性尚不清楚。在本研究中，我们在野生型和维生素D受体（VDR）基因敲低小鼠中建立了[病菌名称未提及]感染模型，并分析了维生素D的作用及其潜在机制。
VDR野生型和VDR基因敲低小鼠经胃内接种[病菌名称未提及]SS1菌株。在确认[病菌名称未提及]感染后，用不同剂量的维生素D对小鼠进行治疗。使用菌落形成试验对胃组织中的感染水平进行定量，并通过免疫组织化学和蛋白质印迹分析胃黏膜中VDR和cathelicidin抗菌肽（CAMP）的表达水平。
VDR基因敲低小鼠的胃黏膜比VDR野生型小鼠更容易受到[病菌名称未提及]定植，且VDR和CAMP表达水平更低。[病菌名称未提及]感染上调了野生型和突变型小鼠胃中VDR和CAMP的表达，维生素D治疗导致VDR和CAMP水平进一步升高，同时显著且剂量依赖性地降低了两组小鼠的[病菌名称未提及]定植率，且不影响血钙或血磷水平。
我们的数据表明，口服维生素D可降低[病菌名称未提及]定植率，并上调胃黏膜中VDR和CAMP的表达，提示VitD/VDR/CAMP信号通路在清除胃内[病菌名称未提及]中发挥作用。这些发现为维生素D的抗菌活性机制提供了重要见解，应有助于制定根除[病菌名称未提及]的措施。
