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Neutrophil activation by Helicobacter pylori

C Mooney1, J Keenan, D Munster

  • 1University Department of Surgery, Christchurch School of Medicine, New Zealand.

Gut
|August 1, 1991
PubMed

Insights

Helicobacter pylori secretes a substance, likely N-formyl-methionyl-leucyl-phenylalanine (FMLP), that activates human polymorphonuclear leukocytes (PMNLs). Immune complexes of H. pylori and antibodies further enhance this PMNL activation, potentially causing gastritis.

Area of Science:

  • Immunology
  • Microbiology
  • Gastroenterology

Background:

  • Helicobacter pylori infection leads to persistent polymorphonuclear leukocyte (PMNL) infiltration in the gastric mucosa.
  • Understanding the interaction between H. pylori and host immune cells is crucial for explaining associated gastritis.

Purpose of the Study:

  • To investigate the activation of human PMNLs by substances produced by H. pylori.
  • To determine the role of H. pylori-derived products and immune complexes in PMNL activation and gastric inflammation.

Main Methods:

  • Stimulation of human PMNLs with filtered H. pylori conditioned media and purified H. pylori components.
  • Measurement of PMNL oxidative burst response.
  • High-pressure liquid chromatography (HPLC) to identify active substances.
  • Evaluation of the effect of H. pylori opsonized with anti-H. pylori plasma on PMNL activation.

Main Results:

  • Filtered H. pylori conditioned media induced a significant PMNL oxidative burst, comparable to N-formyl-methionyl-leucyl-phenylalanine (FMLP).
  • A fraction from H. pylori extract stimulated PMNLs and cross-reacted antigenically with FMLP.
  • Opsonized H. pylori prolonged the FMLP-induced oxidative burst, while unopsonized bacteria did not significantly activate PMNLs.
  • Combined H. pylori conditioned media and anti-H. pylori plasma prolonged the FMLP-induced response.

Conclusions:

  • H. pylori synthesizes and secretes a substance, likely FMLP, contributing to PMNL recruitment in gastric infections.
  • Immune complexes of H. pylori antigens and specific antibodies potentiate the PMNL oxidative burst.
  • The interplay between H. pylori products, host PMNLs, and antibodies may drive mucosal damage in H. pylori-associated gastritis.

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