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Related Experiment Videos

Complement and experimental respiratory failure.

P A Ward, K J Johnson, G O Till

    Intensive Care Medicine
    |January 1, 1986
    PubMed
    Summary
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    Lung injury from complement activation involves oxygen free radicals. Protecting against these radicals, like hydroxyl radical, can prevent lung damage, offering insights for conditions such as acute respiratory distress syndrome.

    Area of Science:

    • Pulmonary Medicine
    • Immunology
    • Cellular Biology

    Background:

    • Complement system activation in the lung can cause acute damage and dysfunction.
    • Lung injury is linked to complement-induced generation of oxygen free radicals from neutrophils and macrophages.
    • Myeloperoxidase conversion of hydrogen peroxide to hypochlorous acid may also contribute to lung injury.

    Purpose of the Study:

    • To investigate the role of oxygen radicals in complement-mediated lung injury.
    • To explore the mechanisms by which neutrophils and macrophages contribute to lung damage.
    • To evaluate the protective effects of radical scavengers and formation inhibitors against lung injury.

    Main Methods:

    • Utilizing various experimental models of lung injury.

    Related Experiment Videos

  • Investigating the effects of complement activation, immune complexes (IgG and IgA), neutrophils, and macrophages.
  • Assessing the impact of oxygen radicals, including hydroxyl radical, and myeloperoxidase activity.
  • Testing the efficacy of hydroxyl radical scavengers, catalase, and iron chelators in preventing lung injury.

    • Main Results:

    • Complement-induced lung injury involves oxygen-derived free radicals from neutrophils and macrophages.
    • Exposure to oxygen radicals from complement-activated neutrophils causes endothelial cell damage and necrosis.
    • IgG immune complex-induced lung injury is complement, neutrophil, and oxygen radical-dependent.
    • IgA immune complex-induced lung injury is complement-dependent, oxygen radical-mediated, but neutrophil-independent.
    • Oxygen radicals can directly cause tissue toxicity and potentiate leukocytic proteases.
    • Lung injury in these models is preventable with hydroxyl radical scavengers or formation inhibitors.

    Conclusions:

    • Oxygen radicals play a significant role in complement-mediated lung injury.
    • Different immune complexes elicit distinct pathways of complement-induced lung injury.
    • Therapeutic strategies targeting oxygen radical formation or activity show promise for preventing lung injury.
    • Findings have potential clinical relevance for conditions like adult respiratory distress syndrome.