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Autooxidation as a basis for altered function by polymorphonuclear leukocytes

R L Baehner, L A Boxer, J M Allen

    Blood
    |August 1, 1977
    PubMed
    Summary
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    Human immune cells, polymorphonuclear leukocytes (PMN), may harm themselves with hydrogen peroxide (H2O2), impairing their ability to fight infection. Vitamin E may protect these cells from this self-inflicted damage.

    Area of Science:

    • Immunology
    • Cell Biology
    • Biochemistry

    Background:

    • Human polymorphonuclear leukocytes (PMN) produce reactive oxygen species, including hydrogen peroxide (H2O2), during immune responses.
    • The potential for these reactive oxygen species to cause autotoxicity and impair PMN function is not fully understood.

    Purpose of the Study:

    • To investigate if endogenous hydrogen peroxide (H2O2) production by PMN leads to autotoxicity, hindering directed cell movement and phagocytosis.
    • To explore the protective effects of antioxidants, specifically vitamin E (alpha-tocopherol), against H2O2-induced PMN dysfunction.

    Main Methods:

    • Assessed PMN phagocytosis of opsonized particles and directed migration through filters under various conditions (anaerobic, presence of catalase, superoxide dismutase, H2O2, xanthine-xanthine oxidase).

    Related Experiment Videos

  • Studied PMN function in volunteers supplemented with alpha-tocopherol, measuring phagocytosis, bacterial killing, hexose monophosphate shunt activity, H2O2 release, and microtubule-associated responses.
  • Measured superoxide anion (O2-) release from phagocytizing PMN.

    • Main Results:

    • PMN phagocytosis and migration were enhanced by catalase and impaired by H2O2 or a superoxide-generating system, indicating H2O2's inhibitory role.
    • Alpha-tocopherol supplementation resulted in hyperphagocytic PMN but reduced bacterial killing, with diminished H2O2-dependent cellular responses, suggesting reduced H2O2 availability.
    • H2O2-induced damage to microtubules was reduced in vitamin E supplemented PMN, while O2- release remained unaffected.

    Conclusions:

    • Endogenously produced H2O2 can cause autotoxic damage to PMN, attenuating their directed movement and phagocytic capacity.
    • In vivo administration of vitamin E may protect PMN from H2O2-induced autotoxicity by scavenging H2O2, potentially preserving immune cell function.