AUTHOR=Zhou Anni , Li Lei , Zhao Guiping , Min Li , Liu Si , Zhu Shengtao , Guo Qingdong , Liu Chunjie , Zhang Shutian , Li Peng 

TITLE=Vitamin D3 Inhibits Helicobacter pylori Infection by Activating the VitD3/VDR-CAMP Pathway in Mice

JOURNAL=Frontiers in Cellular and Infection Microbiology

VOLUME=10

YEAR=2020

URL=https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2020.566730

DOI=10.3389/fcimb.2020.566730

ISSN=2235-2988

ABSTRACT=<p><italic>Helicobacter pylori</italic> (<italic>H. pylori</italic>) infection is closely associated with the occurrence and development of gastric diseases. Therefore, eliminating <italic>H. pylori</italic> infection should help to prevent gastric diseases. Vitamin D3 (VitD3, 1,25(OH)<sub>2</sub>D<sub>3</sub>) was previously observed to exhibit anti-<italic>H. pylori</italic> infection activity in clinic, but these results were reported in heterogeneous <italic>in vivo</italic> studies without elucidation of the underlying mechanisms. In the present study, we established <italic>H. pylori</italic> infection models in both wild-type and VDR knockdown (VDR<sup>-KD</sup>) mice, which were used to demonstrate that VitD3 inhibits <italic>H. pylori</italic> infection by enhancing the expression of VitD receptor (VDR) and cathelicidin antimicrobial peptide (CAMP). Furthermore, VDR<sup>-KD</sup> mice that exhibited lower VDR expression were more susceptible to <italic>H. pylori</italic> 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-<italic>H. pylori</italic> infection activity of VitD3 at the molecular level in mice and suggest a new avenue for the clinical management of <italic>H. pylori</italic> eradication therapy.</p>