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

被引:141
作者
Byrne, MF
Kerrigan, SW
Corcoran, PA
Atherton, JC
Murray, FE
Fitzgerald, DJ
Cox, DM
机构
[1] Royal Coll Surgeons Ireland, Dept Clin Pharmacol, Dublin 2, Ireland
[2] Duke Univ, Med Ctr, Div Gastroenterol, Durham, NC 27706 USA
[3] Univ Nottingham Hosp, Div Gastroenterol, Nottingham NG7 2UH, England
[4] Univ Nottingham Hosp, Inst Infect & Immun, Nottingham NG7 2UH, England
[5] Beaumont Hosp, Dept Gastroenterol, Dublin 9, Ireland
基金
英国医学研究理事会;
关键词
D O I
10.1016/S0016-5085(03)00397-4
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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 GPIbalpha 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 (FcgammaRIIA). 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.
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页码:1846 / 1854
页数:9
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