期刊
JOURNAL OF INFECTIOUS DISEASES
卷 205, 期 8, 页码 1321-1329出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jis180
关键词
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资金
- Ministry of Education, Science and Culture [22591106]
- Osaka Foundation for the Promotion of Clinical Immunology
- St. Lukes Medical Center [05-025]
- Grants-in-Aid for Scientific Research [22591106, 23590542, 22790406, 22000013] Funding Source: KAKEN
Background. The mechanisms of thrombocytopenia and platelet phagocytosis in dengue illness are not fully understood. Methods. A prospective hospital-based study was conducted to examine the relationships between platelet counts, serum thrombopoietin (TPO) levels, and platelet apoptosis and phagocytosis in 81 patients with secondary dengue virus (DV) infections and 38 healthy volunteers. The apoptosis and phagocytosis of cultured platelets after exposure to DV were also examined. Results. Platelet apoptosis, platelet phagocytosis, and serum TPO levels were increased significantly in patients during the acute and early convalescence phases compared with levels observed in patients during the convalescence phase and in healthy volunteers. A significant correlation between platelet apoptosis and platelet phagocytosis was also observed in these patients. Platelet phagocytosis was inhibited significantly by the D89E mutant, which carries a point mutation in the RGD motif of milk fat globule-epidermal growth factor 8, a phosphatidylserine-recognizing bridge molecule. DV-induced platelet apoptosis and increased phagocytosis of DV-induced apoptotic platelets was confirmed using in vitro assays. Conclusions. Our data suggest an increased phagocytosis of DV-induced apoptotic platelets by macrophages via a phosphatidylserine-recognizing pathway in secondary DV infection. Accelerated platelet clearance, however, was overcome by TPO-induced enhanced thrombopoiesis in these patients.
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