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Complement-dependent histaminase release from human granulocytes.

J J Herman, I K Rosner, A E Davis

    The Journal of Clinical Investigation
    |June 1, 1979
    PubMed
    Summary
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    Particle-bound C3b triggers enzyme release from human granulocytes, independent of phagocytosis. Eosinophils require particle opsonization for similar enzyme release, suggesting a dual complement role.

    Area of Science:

    • Immunology
    • Biochemistry

    Background:

    • Complement proteins play a crucial role in immune responses.
    • Specific complement components mediate non-cytotoxic enzyme release from immune cells.

    Purpose of the Study:

    • To investigate the role of particle-bound complement proteins in inducing non-cytotoxic enzyme release from human granulocytes.
    • To differentiate the mechanisms of enzyme release in neutrophils versus eosinophils.

    Main Methods:

    • Utilized sera genetically deficient in complement and purified complement components.
    • Assessed enzyme release (histaminase, beta-glucuronidase, arylsulfatase) under conditions excluding fluid-phase complement.
    • Manipulated particle-bound C3b levels and tested the effect of C3b inactivator and fluid-phase C3b.

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    Main Results:

    • Neutrophil enzyme release (histaminase, beta-glucuronidase) was solely dependent on particle-bound C3b and did not require phagocytosis.
    • Enzyme release from neutrophils was proportional to C3b input and inhibited by C3b inactivator or fluid-phase C3b.
    • Eosinophil enzyme release required particle opsonization (by C3b or other proteins) and phagocytosis.

    Conclusions:

    • Particle-bound C3b is a key mediator of non-cytotoxic enzyme release from neutrophils.
    • Complement component C3 has a dual role in vascular permeability: C3a/C5a mediate release of vasoactive mediators, while C3b mediates release of enzymes that inactivate them.
    • Distinct mechanisms govern enzyme release from neutrophils and eosinophils, highlighting cell-specific complement functions.