| Summary: | (1) Background: Persistent <i>Helicobacter pylori</i> infection is the most important risk factor for gastric cancer. The urokinase receptor (uPAR) is upregulated in lesions harboring cancer invasion and inflammation. Circumstantial evidence tends to correlate <i>H. pylori</i> colonization with increased uPAR expression in the human gastric epithelium, but a direct causative link has not yet been established in vivo; (2) Methods: In a mouse model of <i>H. pylori</i>-induced gastritis, we investigated the temporal emergence of uPAR protein expression in the gastric mucosa in response to <i>H. pylori</i> (SS1 strain) infection; (3) Results: We observed intense uPAR immunoreactivity in foveolar epithelial cells of the gastric corpus due to de novo synthesis, compared to non-infected animals. This uPAR induction represents a very early response, but it increases progressively over time as do infiltrating immune cells. Eradication of <i>H. pylori</i> infection by antimicrobial therapy causes a regression of uPAR expression to its physiological baseline levels. Suppression of the inflammatory response by prostaglandin E<sub>2</sub> treatment attenuates uPAR expression. Notwithstanding this relationship, <i>H. pylori</i> does induce uPAR expression in vitro in co-cultures with gastric cancer cell lines; (4) Conclusions: We showed that persistent <i>H. pylori</i> colonization is a necessary event for the emergence of a relatively high uPAR protein expression in murine gastric epithelial cells.
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