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High dose corticosteroids and cell-cell interactions.

B T Kjellström, B Risberg

    Acta Chirurgica Scandinavica. Supplementum
    |January 1, 1985
    PubMed
    Summary
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    Adult Respiratory Distress Syndrome (ARDS) involves inflammation and lung injury. High-dose corticosteroids (HDC) may reduce lung damage by inhibiting polymorphonuclear granulocytes (PMN) aggregation and their harmful interactions with endothelial cells.

    Area of Science:

    • Pulmonary Medicine
    • Immunology
    • Cell Biology

    Background:

    • Adult Respiratory Distress Syndrome (ARDS) is a severe lung condition often resulting from trauma or sepsis.
    • It involves fluid buildup in the lungs due to increased microvascular permeability.
    • Complement system activation, particularly C5a, and polymorphonuclear granulocytes (PMN) are implicated in ARDS pathogenesis.

    Purpose of the Study:

    • To investigate the role of PMN, complement activation, and platelets in ARDS-related endothelial cell (EC) damage.
    • To evaluate the potential protective effects of high-dose corticosteroids (HDC) on these cellular interactions.

    Main Methods:

    • In vitro experiments using cultured EC monolayers exposed to PMN, C5a, oxygen free radicals, and platelet serotonin.
    • Assessment of EC damage, PMN aggregation, adhesion, and serotonin's effects.

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  • Evaluation of HDC's impact on PMN behavior and EC interactions.

    • Main Results:

    • PMN and C5a induced morphological and functional damage to EC monolayers.
    • Oxygen free radicals also caused EC damage, mimicking ARDS conditions.
    • HDC inhibited PMN aggregation and adhesion to ECs, potentially by increasing PMN hydrophobicity and reducing free radical production.
    • Platelet serotonin amplified PMN cytotoxicity and enhanced PMN-EC adhesion.

    Conclusions:

    • Complement-activated PMN contribute to pulmonary microvascular EC injury in ARDS, exacerbated by platelet-derived serotonin.
    • HDC shows promise in mitigating ARDS by reducing harmful PMN-endothelial cell interactions.
    • Targeting PMN activation and aggregation presents a potential therapeutic strategy for ARDS.