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Helicobacter pylori Colonization Drives Urokinase Receptor (uPAR) Expression in Murine Gastric Epithelium During Early Pathogenesis.
Alpízar-Alpízar, Warner; Skindersoe, Mette E; Rasmussen, Lone; Kriegbaum, Mette C; Christensen, Ib J; Lund, Ida K; Illemann, Martin; Laerum, Ole D; Krogfelt, Karen A; Andersen, Leif P; Ploug, Michael.
Afiliação
  • Alpízar-Alpízar W; The Finsen Laboratory, Rigshospitalet, 2100 Copenhagen, Denmark.
  • Skindersoe ME; Biotech Research and Innovation Centre (BRIC), University of Copenhagen, 2100 Copenhagen, Denmark.
  • Rasmussen L; Centre for Research on Microscopic Structures (CIEMic) and Department of Biochemistry, University of Costa Rica, 2060 San José, Costa Rica.
  • Kriegbaum MC; Department of Bacteria, Parasites and Fungi, Statens Serum Institute, 2300 Copenhagen, Denmark.
  • Christensen IJ; Bacthera, Kogle Allé 6, 2970 Hoersholm, Denmark.
  • Lund IK; Department of Clinical Microbiology, Rigshospitalet, 2100 Copenhagen, Denmark.
  • Illemann M; The Finsen Laboratory, Rigshospitalet, 2100 Copenhagen, Denmark.
  • Laerum OD; Biotech Research and Innovation Centre (BRIC), University of Copenhagen, 2100 Copenhagen, Denmark.
  • Krogfelt KA; The Finsen Laboratory, Rigshospitalet, 2100 Copenhagen, Denmark.
  • Andersen LP; Biotech Research and Innovation Centre (BRIC), University of Copenhagen, 2100 Copenhagen, Denmark.
  • Ploug M; Hvidovre Hospital, University of Copenhagen, 2650 Copenhagen, Denmark.
Microorganisms ; 8(7)2020 Jul 09.
Article em En | MEDLINE | ID: mdl-32660136
(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.
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Texto completo: 1 Base de dados: MEDLINE Tipo de estudo: Etiology_studies / Prognostic_studies / Risk_factors_studies Idioma: En Ano de publicação: 2020 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Tipo de estudo: Etiology_studies / Prognostic_studies / Risk_factors_studies Idioma: En Ano de publicação: 2020 Tipo de documento: Article