JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
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Chronic mucosal inflammation of the gastric cardia in gastroesophageal reflux disease is not regulated by FOXP3-expressing T cells.

INTRODUCTION: Chronic inflammation at the cardia occurs in gastroesophageal reflux disease (GERD), as well as in the presence of Helicobacter pylori. Regulatory T cells have been demonstrated for H. pylori-induced gastritis, whereas their role has not been studied in GERD.

METHODS: We prospectively analyzed the expression of FOXP3, a marker of various regulatory T cells, as well as the mucosal transcript levels of TGF-beta1 and IL-10. RNA and protein levels have been determined in cardiac biopsies of 70 patients stratified according to GERD (n = 22), controls (n = 17), and H. pylori (n = 31).

RESULTS: GERD presented with chronic inflammation and reduced FOXP3-mRNA in the cardiac mucosa (-84%), whereas H. pylori-positive patients revealed a 25.1-fold increase of FOXP3 gene expression. These results were verified by the regulatory cytokines IL-10 and TGF-beta1, and by the immunohistochemical detection of intramucosal FOXP3-expressing T cells.

CONCLUSION: Chronic inflammation at the cardia associated with either GERD or H. pylori differs concerning the presence of FOXP3-expressing T cells. In contrast to H. pylori, FOXP3-expressing T cells are not associated with GERD-associated carditis.

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