Cutting edge: urease release by Helicobacter pylori stimulates macrophage inducible nitric oxide synthase.

نویسندگان

  • Alain P Gobert
  • Benjamin D Mersey
  • Yulan Cheng
  • Darren R Blumberg
  • Jamie C Newton
  • Keith T Wilson
چکیده

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 NO(2)(-) production with the ureA(-) strain compared with wild-type and other mutants. Similarly, macrophage NO(2)(-) generation was increased by H. pylori protein water extracts of all strains except ureA(-). Recombinant urease stimulated significant increases in macrophage iNOS expression and NO(2)(-) 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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عنوان ژورنال:
  • Journal of immunology

دوره 168 12  شماره 

صفحات  -

تاریخ انتشار 2002