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Article Abstract
H. pylori causes gastritis and increases the risk of gastric ulcer and gastric cancer. However, it was recently shown that H. pylori provides protection against inflammatory bowel diseases. To assess the molecular mechanism of such functions, we studied the role of DC-SIGN in H. pylori-infected gastrointestinal epithelial cells. DC-SIGN was found to be over-expressed in the gastric epithelial cells infected with H. pylori and mediated Th1 differentiation, which may be involved in H. pylori-induced gastric mucosal injury. In addition, DC-SIGN was also up-regulated in the intestinal epithelial cells derived from colitis mouse model, but the expression levels were blocked upon H. pylori infection, indicating that H. pylori infection may reduce both local and systemic inflammatory responses. In conclusion, we propose that gastrointestinal epithelial cells infected with H. pylori may lead to acquiring of immune properties via a trans-differentiation process, and regulate tissue-associated immune compartments under the control of DC-SIGN.
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