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H. pylori Infection induces a Vitamin D (Vit. D) Immune Response

Thursday, October 11, 2012 — Poster Session IV

2:00 p.m. – 4:00 p.m.

Natcher Conference Center, Building 45




  • JS Joo
  • C Yu
  • M Yan
  • W Chen
  • Y Sun
  • F Chen
  • S Datta
  • A Yang
  • W. G. Coleman


There are few reports indicating a VitD3 immune response to H. pylori infection. We used microarray analysis to monitor host responses to H. pylori infection and found that the vitamin D receptor (VDR) was up-regulated. We tested this observation in the RAW 264.7 cells using Q-PCR, and confirmed that expressions were increased during H. pylori infection. Further, we also observed increased VDR, CYP27B1 and Cathelicidin in resident macrophages isolated from the peritoneal cavity of wild type mice. In contrast, CYP27b1 is down-regulated in resident macrophages isolated from VDR-deficient VDR KO mice. We extended our studies to VDR KO mice to evaluate the role of VDR on the modulation of mucosal immune response to H. pylori infection. H. pylori colonization levels in the gastric mucosa of VDR KO mice was significantly lower compared with wild type littermates. We observed that cytokines RNA expression increased when H. pylori primed dendritic cells were co-cultured with T-cells from VDR KO mice relative to wild type T-cells, especially inflammatory cytokines. These results suggest that during H. pylori infection VitD3 acts as an enhancer of an innate immune response and an inhibitor of adaptive immune responses, thus, contributing to persistent H. pylori colonization.

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