Glucocorticoid-Induced Impairment of Macrophage Antimicrobial Activity: Mechanisms and Dependence on the State of Activation

Schaffner, Andreas; Schaffner, Thomas (1987). Glucocorticoid-Induced Impairment of Macrophage Antimicrobial Activity: Mechanisms and Dependence on the State of Activation. Reviews of infectious diseases, 9(Suppl. 5), S620-S629. The University of Chicago Press 10.1093/clinids/9.Supplement_5.S620

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Experimental observations indicate that tissue macrophages deployed in great numbers at critical anatomic sites such as the liver, spleen, and lung are major targets for glucocorticoids compromising natural resistanceof the host. Therapeutic concentrations ofglucocorticoids appear to prevent destruction of microorganisms ingested by macrophages without interfering with phagocytosis, phagolysosomal fusion, and/or secretion of reactive oxygen intermediates. These findings indicate that at the cellular level the glucocorticoid target should be sought for in the nonoxidative armature of the phagocyte and that nonoxidative killing systems of resident tissue macrophages play an important role in natural resistance to opportunistic pathogens. Glucocorticoids do not prevent lymphokine-induced activation of oxidative killing systems. Thus, lymphokines such as interferon-γ can restore the microbicidal activity of macrophages functionally impaired by glucocorticoids. Counterbalance of the suppressive effect of glucocorticoids by lymphokines might only be possible, however, for pathogens susceptible to oxidative killing and not for microorganisms that are more resistant to reactive oxygen intermediates such as Aspergillus spores and Nocardia, opportunists that appear to be particularly associated with hypercortisolism.

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