Inhibition by dexamethasone of human neutrophil apoptosis in vitro

Nat Immun. 1995 Apr;14(4):198-208.


We investigated in this study the effect of a synthetic glucocorticoid hormone, dexamethasone (Dex), on apoptosis of human peripheral blood neutrophils. Dex inhibited spontaneous and tumor necrosis factor-alpha (TNF-alpha)-induced neutrophil apoptosis in a concentration- and time-dependent manner. This effect of Dex on neutrophil apoptosis was completely reversed by a glucocorticoid receptor antagonist, RU38486, and by cycloheximide. The decrease in sensitivity to TNF-alpha-induced apoptosis cannot be ascribed to a down-modulation of TNF receptors on these cells. These observations suggest that a glucocorticoid hormone participates in the regulation of neutrophil apoptosis and that inhibition of human neutrophil apoptosis by Dex is mediated through glucocorticoid-receptor-induced de novo synthesis of macromolecules. Possible mechanisms and implications of this phenomenon are discussed.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects*
  • Cycloheximide / pharmacology
  • Dexamethasone / pharmacology*
  • Humans
  • Neutrophils / chemistry
  • Neutrophils / cytology*
  • Receptors, Glucocorticoid / antagonists & inhibitors
  • Receptors, Tumor Necrosis Factor / biosynthesis
  • Tumor Necrosis Factor-alpha / immunology


  • Receptors, Glucocorticoid
  • Receptors, Tumor Necrosis Factor
  • Tumor Necrosis Factor-alpha
  • Dexamethasone
  • Cycloheximide