Platelet binding and phagocytosis by macrophages

Bahram A Badlou, Ya Ping Wu, W Martin Smid, Jan-Willem N Akkerman*

*Corresponding author for this work

    Research output: Contribution to journalArticleAcademicpeer-review

    38 Citations (Scopus)


    BACKGROUND: Earlier it was reported that metabolic arrest followed by incubation at 4 degrees C reduces the platelet (PLT) storage defect. Here it is reported that this treatment also reduces binding and phagocytosis by macrophages.

    STUDY DESIGN AND METHODS: Phagocytosis of mepacrine-labeled PLTs by macrophages changes the latter into bright fluorescent particles easily detected by fluorescence-activated cell sorting.

    RESULTS: In combination with conventional binding analysis it was found that binding to phorbol 12-myristate 13-acetate-matured THP-1 cells is primarily regulated by PLT P-selectin expression and phagocytosis by combined phosphatidylserine (PS) exposure and glycoprotein (GP) Ibalpha clustering. It was found that trapping of PLT Ca2+ and raising cAMP reduces phagocytosis by lowering PS exposure. Chilling of PLTs leads to an increase in binding and PS- and GPIbalpha-mediated phagocytosis. Prior depletion of PLT energy stores prevents this increase by preserving low Ca2+ concentration, PS exposure, and PS-mediated phagocytosis.

    CONCLUSION: These data characterize the individual factors that control PLT binding and phagocytosis and might help to define conditions that improve the survival of stored PLTs after transfusion.

    Original languageEnglish
    Pages (from-to)1432-43
    Number of pages12
    Issue number8
    Publication statusPublished - Aug-2006


    • Blood Preservation/adverse effects
    • Cell Line
    • Cell Survival
    • Humans
    • Macrophages/metabolism
    • P-Selectin/metabolism
    • Phagocytosis
    • Platelet Adhesiveness
    • Platelet Transfusion

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