Helicobacter pylori Induces Increased Expression of the Vitamin D Receptor in Immune Responses. Issue 1 (4th November 2013)

• Record Type: Journal Article
• Authors: Guo, Lihua; Chen, Wenguo; Zhu, Huatuo; Chen, Yu; Wan, Xingyong; Yang, Ningmin; Xu, Shuhua; Yu, Chaohui; Chen, Lihua
• Is Part Of: Helicobacter. Volume 19:Issue 1(2014:Feb.)
• Page Start: 37
• Page End: 47
• Publication Date: 2013-11-04
• Subjects: Helicobacter -- Periodicals; Helicobacter infections -- Periodicals; Stomach -- Diseases -- Periodicals; 616.3301405
• DOI: 10.1111/hel.12102
• Languages: English
• ISSNs: 1083-4389

Abstract

<abstract abstract-type="main" id="hel12102-abs-0001"> <title>Abstract</title> <sec id="hel12102-sec-0001" sec-type="section"> <title>Background</title> <p>Vitamin D receptor (VDR) is a member of the nuclear receptor family of transcription factors that play a critical role in innate immunity. This study examined the role of VDR in gastric innate immune defence against the gastric pathogen <italic>Helicobacter pylori</italic>.</p> </sec> <sec id="hel12102-sec-0002" sec-type="section"> <title>Materials and Methods</title> <p>Seventeen <italic>H. pylori</italic>‐infected patients and sixteen controls participated in the study. The GES‐1 cells were transfected with siRNA or incubated with or without 1α, 25(OH)<sub>2</sub>D<sub>3</sub> (100 nmol/L) then infected with <italic>H. pylori</italic>. VDR, cathelicidin antimicrobial protein (CAMP), and cytokine mRNA expression levels in normal and <italic>H. pylori</italic>‐infected gastric mucosa and GES‐1 cells was determined by qRT‐PCR and correlated with the histopathologic degree of gastritis. Bactericidal activity was measured by using a colony‐forming unit assay.</p> </sec> <sec id="hel12102-sec-0003" sec-type="section"> <title>Results</title> <p>Vitamin D receptor mRNA expression levels were significantly upregulated in <italic>H. pylori</italic>‐infected patients and positively correlated with chronic inflammation scores. There was a significant positive correlation between VDR and CAMP mRNA expression in <italic>H. pylori‐</italic>positive gastric mucosa. VDR siRNA reduced <italic>H. pylori‐</italic>induced CAMP production and conversely increased IL‐6 and IL8/CXCL8 expression levels. The vitamin D agonist 1α, 25(OH)<sub>2</sub>D<sub>3</sub> increased CAMP expression and reduced cytokine activation in GES‐1 cells infected with <italic>H. pylori</italic>. 1α, 25(OH)<sub>2</sub>D<sub>3</sub> could enhance the intracellular killing of the replicating bacteria, but the presence of siVDR and siCAMP led to a decline in its bactericidal ability.</p> </sec> <sec id="hel12102-sec-0004" sec-type="section"> <title>Conclusions</title> <p>The expression of VDR and CAMP in the gastric epithelium is up‐regulated in the case of <italic>H. pylori</italic> infection; thus, VDR plays an important role in gastric mucosa homeostasis and host protection from <italic>H. pylori</italic> infection.</p> </sec> </abstract>