Inhibition of granulocyte function by steroids is not limited to corticoids. Studies with sex steroids.
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.
D000305:Adrenal Cortex Hormones / Q000494:pharmacology*; D002449:Cell Aggregation / Q000187:drug effects; D002462:Cell Membrane / Q000187:drug effects; D002478:Cells, Cultured; D006098:Granulocytes / Q000166:cytology / Q000187:drug effects*; D006801:Humans; D008776:Methylprednisolone Hemisuccinate / Q000494:pharmacology; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology
D000305:Adrenal Cortex Hormones; D009240:N-Formylmethionine Leucyl-Phenylalanine; D008776:Methylprednisolone Hemisuccinate