Inhibition of granulocyte function by steroids is not limited to corticoids. Studies with sex steroids

• Published in: Inflammation 1988-06, Vol.12 (3), p.277-284
• Main Authors: HAMMERSCHMIDT, D. E, KNABE, A. C, SILBERSTEIN, P. T, LAMCHE, H. R, COPPO, P. A
• Format: Article
• Language: English
• Subjects: Adrenal Cortex Hormones - pharmacology; Biological and medical sciences; Cell Aggregation - drug effects; Cell Membrane - drug effects; Cells, Cultured; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Genetics of the immune response; Granulocytes - cytology; Granulocytes - drug effects; Humans; Immunobiology; Methylprednisolone Hemisuccinate - pharmacology; N-Formylmethionine Leucyl-Phenylalanine - pharmacology
• ISSN: 0360-3997; 1573-2576
• DOI: 10.1007/BF00920079

Noting that corticosteroid doses required for protection in shock models exceeded those required to saturate glucocorticoid receptors in mammalian cells, we postulated a nonspecific physicochemical effect of steroids upon the cell membrane, and therefore tested three noncorticoid steroids for their effects on granulocyte function. All three (conjugated equine estrogen, a synthetic progestogen, and a synthetic androgen) behaved in manner analogous to corticoids at similar concentrations, inhibiting granulocyte aggregation, chemotaxis, and chemiluminescence, as well as binding to the granulocytes of the synthetic oligopeptide agonist f-Met-Leu-Phe. Estrogen was further shown to reduce granulocyte membrane fluidity, assessed by electron paramagnetic resonance. We propose that the unique effects of extremely high-dose corticosteroids are not mediated via the glucocorticoid receptor, but result rather from physicochemical effects of the drugs upon the membranes of effector cells.