Helicobacter pylori Colonization Drives Urokinase Receptor (uPAR) Expression in Murine Gastric Epithelium During Early Pathogenesis
artículo original
Fecha
2020Autor
Alpízar Alpízar, Warner
Skindersoe, Mette Elena
Rasmussen, Lone
Kriegbaum, Mette Camila
Christensen, Ib J.
Lund, Ida Katrine
Illemann, Martin
Laerum, Ole Didrik
Krogfelt, Karen Angeliki
Andersen, Leif Percival
Ploug, Michael
Metadatos
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(1) Background: Persistent Helicobacter pylori 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 H. pylori 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 H. pylori-induced gastritis, we investigated
the temporal emergence of uPAR protein expression in the gastric mucosa in response to H. pylori
(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 H. pylori infection by antimicrobial therapy causes a regression of
uPAR expression to its physiological baseline levels. Suppression of the inflammatory response by
prostaglandin E2 treatment attenuates uPAR expression. Notwithstanding this relationship, H. pylori
does induce uPAR expression in vitro in co-cultures with gastric cancer cell lines; (4) Conclusions: We
showed that persistent H. pylori colonization is a necessary event for the emergence of a relatively
high uPAR protein expression in murine gastric epithelial cells.
External link to the item
10.3390/microorganisms8071019Colecciones
- Biología [1616]