Open AccessRole of virulence factors, cell components and adhesion in Helicobacter pylori ‐mediated iNOS induction in murine macrophages
Author(s) -
Assmann Ilka A.,
Enders Georg A.,
Püls Jürgen,
Rieder Gabriele,
Haas Rainer,
Hatz Rudolf A.
Publication year - 2001
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2001.tb01561.x
Subject(s) - virulence , biology , helicobacter pylori , microbiology and biotechnology , lipopolysaccharide , mutant , virulence factor , phagocytosis , bacterial outer membrane , nitric oxide synthase , macrophage , helicobacter , nitric oxide , gene , immunology , escherichia coli , genetics , in vitro , endocrinology
To investigate the mechanisms involved in Helicobacter pylori ‐mediated inducible nitric oxide synthase (iNOS) upregulation in mononuclear cells we cocultivated human THP‐1 acute monocytic leukemia cells and murine J774A.1 professional macrophages with different H. pylori wild‐type strains and mutants. We have shown that H. pylori ‐mediated iNOS induction in J774A.1 is independent of established virulence factors but dependent on direct interaction between bacteria and cells. In J774A.1, iNOS was equally upregulated by the wild‐type strains J99, 26695, P12, and P1 as well as by mutants lacking the cag pathogenicity island, vacA, katA , alpAB genes and the hp0043 gene taking part in lipopolysaccharide biosynthesis when direct cell contact was allowed but not when bacteria and cells were separated by protein‐permeable filter membranes. In contrast, iNOS was not induced in THP‐1. This indicates that H. pylori ‐mediated iNOS induction in J774A.1 is independent of important virulence factors whereas cell contact is crucial which suggests a role of adhesion or phagocytosis.