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Related Experiment Videos

Platelet modulation of polymorphonuclear leukocyte shear induced aggregation.

B G Rhee, E R Hall, L V McIntire

    Blood
    |January 1, 1986
    PubMed
    Summary

    Platelets modulate polymorphonuclear leukocyte (PMNL) aggregation under shear stress, mediated by lipoxygenase activity. This interaction highlights a potential cooperation between platelets and leukocytes in shear-induced aggregation.

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    Area of Science:

    • Hematology
    • Cellular Biology
    • Biochemistry

    Background:

    • Polymorphonuclear leukocytes (PMNLs) play a crucial role in inflammatory responses.
    • Platelet activation and aggregation are central to hemostasis and thrombosis.
    • Understanding cell-cell interactions under shear stress is vital for cardiovascular and inflammatory research.

    Purpose of the Study:

    • To investigate the role of platelets in shear-induced PMNL aggregation.
    • To identify the molecular mechanisms, specifically lipoxygenase pathways, involved in this interaction.
    • To explore the potential cooperation between platelets and leukocytes under physiological shear conditions.

    Main Methods:

    • Cone and plate viscometry was used to apply controlled shear stress.
    • Coulter Counter analysis quantified PMNL aggregation using the large-particle percentage (LPP).

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  • Inhibitors of cyclo-oxygenase and lipoxygenase pathways were employed, alongside reversed-phase high-performance liquid chromatography (RP-HPLC) to analyze lipoxygenase products.

    • Main Results:

    • PMNLs alone did not aggregate under shear stress below 150 dynes/cm2.
    • Platelet-rich plasma significantly enhanced PMNL aggregation under shear stress.
    • Lipoxygenase inhibitors (nordihydroguaiaretic acid and U-60257) suppressed shear-induced PMNL aggregation, while cyclo-oxygenase inhibition (acetylsalicylic acid) did not.
    • Formation of lipoxygenase products (5-HETE, 12-HETE, 15-HETE, LTB4) was confirmed.

    Conclusions:

    • Platelets modulate shear-induced PMNL aggregation.
    • This modulation is dependent on C-5 and/or C-12 lipoxygenase activity.
    • A cooperative mechanism between platelets and leukocytes in response to shear stress, involving lipoxygenase pathways, is supported.