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Related Experiment Videos

In vitro macrophage manifestation of cortisone-induced decrease in resistance to mouse hepatitis virus.

C E Taylor, W Y Weiser, F B Bang

    The Journal of Experimental Medicine
    |March 1, 1981
    PubMed
    Summary

    Corticosteroids like hydrocortisone can increase macrophage susceptibility to MHV (PRI) virus in mice. This effect, observed in resistant macrophages, can be reversed by spleen cell factors.

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    Area of Science:

    • Immunology
    • Virology
    • Endocrinology

    Background:

    • Genetically resistant C3H mice normally produce macrophages resistant to MHV (PRI) virus.
    • Macrophage susceptibility to viral infections can be influenced by various factors, including host treatments.

    Purpose of the Study:

    • To investigate the effect of corticosteroid administration on macrophage susceptibility to MHV (PRI) in resistant mice.
    • To explore the role of spleen cells in modulating this susceptibility.

    Main Methods:

    • Treatment of C3H mice with hydrocortisone, dexamethasone, prednisolone, progesterone, or testosterone.
    • In vitro culture of macrophages from treated mice.
    • Assessment of macrophage susceptibility to MHV (PRI) virus.
    • Co-culture experiments with spleen cells from treated mice.

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    Main Results:

    • Hydrocortisone, dexamethasone, and prednisolone treatment increased macrophage susceptibility to MHV (PRI) in vitro.
    • Progesterone and testosterone did not affect susceptibility.
    • Spleen cells from cortisone-treated mice enhanced susceptibility of resistant macrophages by 100-fold.
    • Concanavalin A-treated spleen cell supernatant reversed hydrocortisone-induced susceptibility.

    Conclusions:

    • Corticosteroids can overcome genetic resistance in macrophages, increasing susceptibility to MHV (PRI).
    • Spleen cells play a role in modulating macrophage antiviral susceptibility, potentially through soluble factors.