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Ionophore-induced functional changes in macrophages.

G Fóris, G A Medgyesi, G Füst

    Immunobiology
    |May 1, 1984
    PubMed
    Summary
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    Calcium ionophores A 23187 and valinomycin activate rat peritoneal macrophages, but inhibit Fc receptor-mediated functions. These ionophores impair effector functions at non-toxic concentrations.

    Area of Science:

    • Immunology
    • Cell Biology
    • Pharmacology

    Background:

    • Ionophores modulate cation transport across cell membranes.
    • Calcium (Ca2+) and potassium (K+) ion fluxes are critical for macrophage function.
    • Peritoneal macrophages (PM) play a key role in innate and adaptive immunity.

    Purpose of the Study:

    • To investigate the effects of Ca2+ and K+ ionophores on rat peritoneal macrophage activation and effector functions.
    • To determine the role of extracellular calcium in ionophore-induced effects.

    Main Methods:

    • Treatment of rat peritoneal macrophages with Ca ionophore A 23187 and K+ ionophore valinomycin at varying concentrations.
    • Assessment of macrophage activation through aggregation, nitro blue tetrazolium (NBT) reduction, superoxide anion production, and beta-glucuronidase release.

    Related Experiment Videos

  • Measurement of lactate dehydrogenase (LDH) release to assess cytotoxicity.
  • Evaluation of Fc receptor (FcR) and C3bR-mediated phagocytosis, intracellular killing, and antibody-dependent cellular cytotoxicity (ADCC).
  • Investigation of the role of extracellular calcium using EGTA.

    • Main Results:

    • Both A 23187 and valinomycin induced activation-related changes in PM, including aggregation and release of inflammatory mediators.
    • A 23187-induced activation was dependent on extracellular Ca2+, while valinomycin's effect was not.
    • FcR-mediated functions (incorporation, intracellular killing, ADCC) were significantly inhibited by both ionophores.
    • C3bR-mediated phagocytosis showed greater resistance to ionophore treatment.
    • Inhibition of effector functions occurred at non-toxic ionophore concentrations and did not require extracellular Ca2+ during exposure.

    Conclusions:

    • Cation ionophores can differentially modulate macrophage activation and effector functions.
    • Modulation of intracellular cation levels by ionophores significantly impairs FcR-dependent immune responses.
    • These findings highlight the complex role of cation homeostasis in macrophage effector mechanisms and suggest potential therapeutic targets.