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Complement and endotoxin-induced lung injury in sheep.

J K Horn, I M Goldstein, M R Flick

    The Journal of Surgical Research
    |May 1, 1984
    PubMed
    Summary

    Endotoxin infusions in sheep trigger lung injury by increasing microvascular permeability. Complement C5-derived peptides in plasma and lymph attract polymorphonuclear leukocytes, contributing to this lung injury.

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    Area of Science:

    • Pulmonary Medicine
    • Immunology
    • Critical Care Medicine

    Background:

    • Endotoxin infusions in sheep induce lung injury with increased microvascular permeability, mimicking human sepsis-induced acute respiratory distress syndrome.
    • This lung injury may involve interactions between complement activation products and polymorphonuclear leukocytes.

    Purpose of the Study:

    • To investigate the role of complement-derived chemotactic factors in endotoxin-induced lung injury.
    • To determine if endotoxin stimulates the generation of chemotactic activity for polymorphonuclear leukocytes in sheep.

    Main Methods:

    • Sheep were infused with Escherichia coli endotoxin.
    • Plasma and lung lymph were collected and analyzed for chemotactic activity for polymorphonuclear leukocytes.
    • Chemotactic activity was assessed for heat stability and sensitivity to C5 antibodies.

    Main Results:

    • Endotoxin infusion led to increased lung lymph fluid and protein flow, indicating permeability edema.
    • Significant chemotactic activity for polymorphonuclear leukocytes appeared in plasma and lung lymph post-endotoxin infusion.
    • The observed chemotactic activity was heat-stable and neutralized by C5 antibodies.

    Conclusions:

    • Endotoxin administration generates C5-derived peptides in plasma and lung lymph.
    • These C5-derived peptides exhibit chemotactic activity for polymorphonuclear leukocytes.
    • C5-derived peptides likely contribute to pulmonary leukostasis and endothelial injury, causing permeability edema in endotoxin-induced lung injury.

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