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

2003; Elsevier BV; Volume: 124; Issue: 7 Linguagem: Inglês

10.1016/s0016-5085(03)00397-4

1528-0012

Michael F. Byrne, Steven W. Kerrigan, Paul A. Corcoran, John C. Atherton, Frank E. Murray, Desmond J. Fitzgerald, Dermot Cox,

Autoimmune Bullous Skin Diseases

Background & Aims:Clinical studies have suggested an association between cardiovascular disease and infection with Helicobacter pylori. We examined the effect of H. pylori on platelets and the mechanism of the interaction.Methods:Three of 5 strains of H. pylori induced platelet aggregation with a lag time of 5 ± 2 minutes that was independent of the toxigenic genes cagA and vacA. Aggregation was inhibited completely by aspirin and a glycoprotein (GP) IIb/IIIa antagonist. Aggregation also was inhibited by monoclonal antibodies that prevented the von Willebrand factor (vWF) interaction with GPIb. vWF-coated H. pylori bound to cells transfected with GPIbα but not to mock transfected cells and this was inhibited by an antibody to GPIb.Results:The interaction with platelets appeared to be mediated by vWF because platelet aggregation was blocked by an antibody to vWF. Moreover, a strain of H. pylori that induced platelet aggregation bound vWF to a greater extent than a nonaggregating strain. Aggregation also required IgG and could be inhibited by an antibody to the platelet IgG receptor (FcγRIIA).Conclusions:Some strains of H. pylori induce platelet activation mediated by H. pylori-bound vWF interacting with GPIb, and supported by IgG. These platelet-H. pylori interactions may contribute to the pathogenesis of H. pylori-associated peptic ulcer disease and to the association between H. pylori infection and cardiovascular disease, whereas local platelet effects may contribute to the pathogenesis of H. pylori-associated peptic ulcer disease.