| Autor: |
Bimczok D; Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA., Kao JY; Division of Gastroenterology, Department of Internal Medicine, University of Michigan Health System, Ann Arbor, Michigan, USA., Zhang M; Division of Gastroenterology, Department of Internal Medicine, University of Michigan Health System, Ann Arbor, Michigan, USA., Cochrun S; Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA., Mannon P; Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA., Peter S; Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA., Wilcox CM; Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA., Mönkemüller KE; Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA., Harris PR; Department of Pediatrics, Gastroenterology and Nutrition, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile., Grams JM; Department of Surgery, University of Alabama at Birmingham, Birmingham, Alabama, USA., Stahl RD; Department of Surgery, University of Alabama at Birmingham, Birmingham, Alabama, USA., Smith PD; 1] Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA [2] VA Medical Center Research Service, Birmingham, Alabama, USA., Smythies LE; Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA. |
| Abstrakt: |
Despite the high prevalence of chronic gastritis caused by Helicobacter pylori, the gastric mucosa has received little investigative attention as a unique immune environment. Here, we analyzed whether retinoic acid (RA), an important homeostatic factor in the small intestinal mucosa, also contributes to gastric immune regulation. We report that human gastric tissue contains high levels of the RA precursor molecule retinol (ROL), and that gastric epithelial cells express both RA biosynthesis genes and RA response genes, indicative of active RA biosynthesis. Moreover, primary gastric epithelial cells cultured in the presence of ROL synthesized RA in vitro and induced RA biosynthesis in co-cultured monocytes through an RA-dependent mechanism, suggesting that gastric epithelial cells may also confer the ability to generate RA on gastric dendritic cells (DCs). Indeed, DCs purified from gastric mucosa had similar levels of aldehyde dehydrogenase activity and RA biosynthesis gene expression as small intestinal DCs, although gastric DCs lacked CD103. In H. pylori-infected gastric mucosa, gastric RA biosynthesis gene expression was severely disrupted, which may lead to reduced RA signaling and thus contribute to disease progression. Collectively, our results support a critical role for RA in human gastric immune regulation. |
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