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Harvesting Murine Alveolar Macrophages and Evaluating Cellular Activation Induced by Polyanhydride Nanoparticles
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Published on: June 8, 2012

Phagocytosis-induced injury of normal and activated alveolar macrophages

M P McGee, Q N Myrvik

    Infection and Immunity
    |December 1, 1979
    PubMed

    Insights

    BCG-sensitized macrophages are more vulnerable to cell death when engulfing particles. This increased susceptibility to macrophage injury is linked to free radical activity and phagocytosis.

    Area of Science:

    • Immunology
    • Cell Biology
    • Pathology

    Background:

    • Macrophages play a crucial role in immune responses.
    • Bacillus Calmette-Guérin (BCG) is used as a vaccine and in cancer immunotherapy.
    • Macrophage activation can alter their susceptibility to injury.

    Purpose of the Study:

    • To investigate if BCG-activated macrophages are susceptible to injury upon phagocytosis of particulates.
    • To explore the mechanisms underlying BCG-induced macrophage cytotoxicity.

    Main Methods:

    • Alveolar macrophages were obtained from BCG-sensitized and normal animals.
    • Macrophages were incubated in vitro with BCG or zymosan.
    • Phagocytosis was inhibited using cytochalasin B.
    • Protective effects of antioxidants (catalase, cytochrome c, ascorbic acid) were assessed.

    Main Results:

    • BCG-sensitized macrophages exhibited increased cell death after phagocytosis of BCG or zymosan compared to controls.
    • Inhibition of phagocytosis abrogated the increased cell death.
    • Antioxidants provided partial protection, indicating a role for free radicals.
    • Varied susceptibility among alveolar cell populations suggested heterogeneity or multi-cell type involvement.

    Conclusions:

    • BCG-activated macrophages are susceptible to injury from phagocytosing certain particulates.
    • Phagocytosis and free radical generation are key mechanisms in BCG-induced macrophage cytotoxicity.
    • Alveolar macrophage populations may be heterogeneous, influencing susceptibility to necrosis.

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