pylori infection. According to a case–control study, the average concentration of vitamin D in subjects with autoimmune gastritis was 9.8 ± 5.6 ng/mL; nonspecific gastritis patients, 22.2 ± 13.5 ng/mL; and H. pylori gastritis patients, 11.3 ± 8.4 ng/mL [24]. However,

another Nutritional Deficiencies investigation showed that the 25-OH vitamin D3 levels did not differ between H. pylori+ and H. pylori− patients (p > .20) [25]. Unfortunately, in our study, we were unable to obtain samples promptly to test the concentration of vitamin D. However, we were able to confirm that the vitamin D agonist 1α,25(OH)2D3 had in vitro antimicrobial activity against H. pylori. In our study, we found that 1α,25(OH)2D3 leads to a decrease in IL-6

and IL8/CXCL8 levels. Similar to this, 1α,25(OH)2D3 was found to suppress the production selleck inhibitor of a spectrum of inflammatory cytokines in immune and other cells (such as keratinocytes), including IL-1, IL-2, IL-6, IL8/CXCL8 (29), INF-γ, and TNF-α [26]; this action forms the basis for its anti-inflammatory mechanism. Therefore, 1α,25(OH)2D3 is a marker of systemic inflammation in H. pylori infection. Moreover, 1α,25(OH)2D3 is involved in anti-inflammatory action through its agonistic effect on VDR, which selleck kinase inhibitor targets the antimicrobial peptide CAMP gene in GES-1 cells. Taken together, our data show that 1α,25(OH)2D3 has multiple effects on the expression and release of antimicrobial peptides. We also found that the effects of 1α,25(OH)2D3 on the expression of VDR, CAMP, DEFB4 and CYP24A1. Similar to this, DEFB4 has been shown to be upregulated under

H. pylori infection-associated inflammatory conditions in vivo and under cagA-positive H. pylori infection in AGS cells in vitro [27]; moreover, the DEFB4 promoter contains 17-DMAG (Alvespimycin) HCl VDREs [28]. In agreement with all these findings, 1α,25(OH)2D3 is known to regulate anti-inflammatory activity and other facets of immunity, including the induction of innate immune responses [7, 29]. In conclusion, this study has shown that VDR has an effect on antimicrobial activity against H. pylori. Our data are consistent with and explain at least in part, the critical role of the VDR/CAMP pathway in innate immunity. Moreover, these findings help improve our understanding of the anti-inflammatory mechanism of vitamin D. Given the importance of this subject, more studies are warranted to further understand the functional significance as well as the molecular mechanisms underlying this role of VDR. This study was supported by National Natural Science Foundation of China (No. 30600281) and National 973 Program (2013CB911303). Competing interests: The authors have no financial conflicts of interest. All the coauthors of this paper have contributed to the intellectual content of the paper. “
“Motility mediated by the flagella of Helicobacter pylori is important for the cells to move toward the gastric mucus in niches adjacent to the epithelium; then, H.