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Cutting Edge: Urease Release by Helicobacter pylori Stimulates Macrophage Inducible Nitric Oxide Synthase¹

Alain P. Gobert^*,, Benjamin D. Mersey^*,, Yulan Cheng^*,, Darren R. Blumberg^*,, Jamie C. Newton^* and Keith T. Wilson^2,*,,

^* Department of Medicine, Division of Gastroenterology, and Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD 21201; and Veterans Affairs Maryland Health Care System, Baltimore, MD 21201

Inducible NO synthase (iNOS) expression and production of NO are both up-regulated with Helicobacter pylori infection in vivo and in vitro. We determined whether major pathogenicity proteins released by H. pylori activate iNOS by coculturing macrophages with wild-type or mutant strains deficient in VacA, CagA, picB product, or urease (ureA^-). When filters were used to separate H. pylori from macrophages, there was a selective and significant decrease in stimulated iNOS mRNA, protein, and NO₂^- production with the ureA^- strain compared with wild-type and other mutants. Similarly, macrophage NO₂^- generation was increased by H. pylori protein water extracts of all strains except ureA^-. Recombinant urease stimulated significant increases in macrophage iNOS expression and NO₂^- production. Taken together, these findings indicate a new role for the essential H. pylori survival factor, urease, implicating it in NO-dependent mucosal damage and carcinogenesis.

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