title: P-selectin-dependent platelet aggregation and apoptosis may explain the decrease in platelet count during Helicobacter pylori infection.
abstract: P-selectin expression has been shown in Helicobacter pylori-infected persons, an infection that has been clinically associated with platelet-related diseases, such as idiopathic thrombocytopenic purpura. However, the role of P-selectin expression during H pylori infection remains unclear. In this study, we hypothesized that P-selectin expression was associated with platelet aggregation during H pylori infection. Using flow cytometry, we examined the levels of adhesion between H pylori and platelets as well as the levels of P-selectin expression and platelet phosphatidylserine (PS) expression during H pylori infection. Significantly high levels of adhesion between pro-aggregatory bacteria and platelets were observed. We identified that H pylori IgG is required for bacteria to induce P-selectin expression and that a significant release of P-selectin is essential for H pylori to induce aggregation. In addition, cellular apoptotic signs, such as membrane blebbing, were observed in platelet aggregates. PS expression was also detected in platelets during infection with both pro-aggrogatory and nonaggregatory strains of H pylori. These results suggest that the decrease in platelet counts seen during H pylori infection is the result of P-selection-dependent platelet aggregation and PS expression induced by the bacteria.
authors.affiliation: Institute of Biomedical Sciences, Sun Yat-Sen University, Kaohsiung, Taiwan.
authors.forename: Jeng-Jung
authors.initials: JJ
authors.lastname: Yeh
authors.forename: Sharon
authors.initials: S
authors.lastname: Tsai
authors.forename: Deng-Chyang
authors.initials: DC
authors.lastname: Wu
authors.forename: Jeng-Yih
authors.initials: JY
authors.lastname: Wu
authors.forename: Ta-Chih
authors.initials: TC
authors.lastname: Liu
authors.forename: Angela
authors.initials: A
authors.lastname: Chen
mesh_terms: D000907:Antibodies, Bacterial / Q000097:blood; D017209:Apoptosis / Q000502:physiology; D001422:Bacterial Adhesion / Q000502:physiology; D001792:Blood Platelets / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology* / Q000648:ultrastructure; D016022:Case-Control Studies; D022081:Cell Surface Extensions / Q000648:ultrastructure; D016481:Helicobacter Infections / Q000097:blood* / Q000276:immunology / Q000382:microbiology; D016480:Helicobacter pylori / Q000276:immunology / Q000472:pathogenicity / Q000502:physiology; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D066298:In Vitro Techniques; D008855:Microscopy, Electron, Scanning; D019007:P-Selectin / Q000097:blood*; D010974:Platelet Aggregation / Q000502:physiology; D010976:Platelet Count; D016553:Purpura, Thrombocytopenic, Idiopathic / Q000209:etiology; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D000907:Antibodies, Bacterial; D007074:Immunoglobulin G; D019007:P-Selectin; D014841:von Willebrand Factor