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Helicobacter pylori binds von Willebrand factor and interacts with GPIb to induce platelet aggregation

Michael F Byrne1, Steven W Kerrigan, Paul A Corcoran

  • 1Department of Clinical Pharmacology, Royal College of Surgeons in Ireland, 123 St. Stephens Green, Dublin 2, Ireland.

Gastroenterology
|June 14, 2003
PubMed
Abstract

Insights

Certain Helicobacter pylori strains trigger platelet aggregation via von Willebrand factor (vWF) and IgG, potentially linking H. pylori infection to cardiovascular disease and peptic ulcers.

Area of Science:

  • Microbiology
  • Hematology
  • Immunology

Background:

  • Clinical studies suggest a link between cardiovascular disease and Helicobacter pylori infection.
  • H. pylori infection is common and associated with various gastrointestinal and extraintestinal conditions.

Purpose of the Study:

  • To investigate the effect of H. pylori on platelet function.
  • To elucidate the mechanism of H. pylori-platelet interaction.

Main Methods:

  • Platelet aggregation assays were performed using different H. pylori strains.
  • Inhibition studies involved aspirin, glycoprotein IIb/IIIa antagonists, and antibodies against von Willebrand factor (vWF) and GPIb.
  • Binding assays assessed H. pylori interaction with vWF and platelet receptors.

Main Results:

  • Three of five H. pylori strains induced platelet aggregation.
  • Aggregation was mediated by H. pylori-bound vWF interacting with platelet GPIb receptors.
  • The process required IgG and was inhibited by aspirin and specific antagonists.

Conclusions:

  • H. pylori can activate platelets through vWF and IgG-mediated pathways.
  • These interactions may contribute to H. pylori-associated cardiovascular disease and peptic ulcer disease pathogenesis.

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