Subacute treatment of rats with dexamethasone reduces ICAM-1 levels on circulating monocytes

Biochem Biophys Res Commun. 1997 Feb 24;231(3):675-8. doi: 10.1006/bbrc.1997.6168.


We report for the first time that in vivo treatment with dexamethasone (DEX) reduces levels of intercellular adhesion molecule-1 (ICAM-1) expression on rat circulating unstimulated monocytes (-55%) and peritoneal macrophages (-26%). This effect was present following sub-acute (5 days) treatment with a low dose (0.1 mg/kg per day), but not after single administration of a high dose (1 mg/kg, -2 h), of the steroid. Both acute and sub-acute treatment with DEX failed to modify either basal or up-regulated CD11b expression on peripheral blood monocytes and neutrophils, elastase release from neutrophils, and beta-glucuronidase release from cultured macrophages. The lack of alteration of CD11b expression on circulating leukocytes suggests that the effect of DEX on ICAM-1 expression is secondary to gene repression rather than a non-specific blockade of cell differentiation. These data promote the concept that different dose-regimens with glucocorticoids affect distinct molecular targets and indicate that clinically-related protocols of DEX may reveal new mechanism(s) of action.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Degranulation / drug effects
  • Cell Membrane / metabolism
  • Dexamethasone / administration & dosage*
  • Dose-Response Relationship, Drug
  • Glucocorticoids / administration & dosage*
  • Intercellular Adhesion Molecule-1 / metabolism*
  • Leukocyte Elastase / metabolism
  • Macrophage-1 Antigen / metabolism
  • Macrophages / drug effects
  • Male
  • Monocytes / metabolism*
  • Neutrophils / drug effects
  • Rats
  • Rats, Sprague-Dawley


  • Glucocorticoids
  • Macrophage-1 Antigen
  • Intercellular Adhesion Molecule-1
  • Dexamethasone
  • Leukocyte Elastase