Abstract
of TGF-beta1 and IL-10 were studied and all data were correlated with histopathological values according to the updated Sydney classification. Results: GERD was associated with a chronic inflammation (P=0.065) and reduced FOXP3-mRNA in the cardiac mucosa (84%) as compared to controls, whereas H. pylori-positive patients revealed a 25.1-fold (P= 0.03) increase of FOXP3 gene expression. These results were confirmed by immunohistochemical analysis of intramucosal FOXP3+ Tregs. The absolute number [0.78+/-0.15 versus 2.65+/-0.44, P<0.001] as well as their proportion among all infiltrating immune cells [2.65+/0.61% versus 8.14+/-1.38%, P<0.001] were significantly reduced in patients with GERD than those infected with H. pylori. Conclusion: The GERD-associated chronic inflammation at the cardia is not associated with an infiltration of FOXP3+ Tregs. The regulation of chronic inflammation in GERD is distinct from the common involvement of FOXP3+ Tregs in other chronic inflammatory diseases of the GI tract as presented for H. pylori infection.
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