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Role of virulence factors, cell components and adhesion in Helicobacter pylori-mediated iNOS induction in murine

I A Assmann1, G A Enders, J Püls

  • 1Department of Surgery, Klinikum Grosshadern, Ludwig-Maximilians-University Munich, Germany.

FEMS Immunology and Medical Microbiology
|March 27, 2001
PubMed

Insights

Helicobacter pylori directly interacts with macrophages to induce nitric oxide synthase (iNOS), independent of bacterial virulence factors. This interaction, crucial for iNOS upregulation, suggests a role for bacterial adhesion or phagocytosis.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Helicobacter pylori (H. pylori) infection is linked to various gastric pathologies.
  • Nitric oxide synthase (NOS) plays a role in immune responses.
  • Mechanisms of H. pylori-induced immune responses require further elucidation.

Purpose of the Study:

  • To investigate the role of direct bacterial-host cell interaction in H. pylori-mediated inducible nitric oxide synthase (iNOS) upregulation.
  • To determine if known H. pylori virulence factors are involved in iNOS induction in mononuclear cells.

Main Methods:

  • Cocultivation of human THP-1 cells and murine J774A.1 macrophages with H. pylori wild-type strains and mutants.
  • Utilized protein-permeable filter membranes to differentiate between direct cell contact and soluble factor-mediated effects.
  • Assessed iNOS upregulation in response to various H. pylori strains and genetic mutants.

Main Results:

  • H. pylori induced iNOS in J774A.1 macrophages, but not in THP-1 cells.
  • iNOS induction in J774A.1 cells was independent of H. pylori strains lacking key virulence factors (cag pathogenicity island, vacA, katA, alpAB, hp0043).
  • Direct cell contact between H. pylori and J774A.1 cells was essential for iNOS induction, while separation by a filter abrogated the effect.

Conclusions:

  • H. pylori-mediated iNOS induction in macrophages is critically dependent on direct bacterial-host cell contact.
  • This induction is independent of major H. pylori virulence factors, suggesting a mechanism involving bacterial adhesion or phagocytosis.
  • Differential responses between macrophage cell lines highlight the complexity of host-pathogen interactions.

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