BACKGROUND: Vitamin D[VitD, 1,25 (OH)D] is known to have immunomodulatory and anti-microbial properties; however, its activity againstis unclear. In this study, we establishedinfection models in wild-type and VitDreceptor (VDR) knockdown mice and analyzed the effects of VitDand their underlying mechanisms.
METHODS: VDRand VDRmice were intragastrically infected with theSS1 strain. After confirmation ofinfection, 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.
RESULTS: The gastric mucosa of VDRmice was more susceptible tocolonization and had lower levels of VDR and CAMP expression than that of VDRmice.infection upregulated VDR and CAMP expression in the stomach of both wild-type and mutant mice, and VitDtreatment resulted in further increase of VDR and CAMP levels, while significantly and dose-dependently decreasing thecolonization rate in both mouse groups, without affecting blood calcium or phosphorus levels.
CONCLUSION: Our data indicate that oral administration of VitDreduces thecolonization rate and upregulates VDR and CAMP expression in the gastric mucosa, suggesting a role for VitD/VDR/CAMP signaling in the eradication ofin the stomach. These findings provide important insights into the mechanism underlying the anti-activity of VitDand should be useful in the development of measures to eradicate.