Betamethasone modulates the biological function of human polymorphonuclear leukocytes

Int Arch Allergy Appl Immunol. 1987;82(3-4):532-4. doi: 10.1159/000234270.

Abstract

We have examined the influence of betamethasone (BT) on cyclic AMP (cAMP) metabolism and lysosomal enzyme release from highly purified (approximately equal to 99%) human polymorphonuclear leukocytes (PMNs). Preincubation (1-24 h) of human PMNs with BT (10(-9)-10(-5) M) had no effect on either cAMP content or on beta-glucuronidase release induced by formyl-containing tripeptide (f-met peptide). Preincubation (16-24 h) of PMNs with BT (10(-8)-10(-7) M) dose-dependently potentiated the cAMP accumulation caused by beta-agonists (isoproterenol), adenosine A2/Ra agonist (NECA), prostaglandin E1 (PGE1) and histamine in PMNs. Similarly, BT potentiated the inhibition of f-met peptide-induced beta-glucuronidase release from human PMNs caused by PGE1 (10(-6) M), histamine (2 X 10(-5) M), NECA (10(-4) M) and isoproterenol (10(-6) M).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenylyl Cyclases / metabolism
  • Betamethasone / pharmacology*
  • Cyclic AMP / metabolism
  • Exocytosis / drug effects
  • Humans
  • Lysosomes / enzymology
  • Neutrophils / drug effects*
  • Neutrophils / metabolism

Substances

  • Betamethasone
  • Cyclic AMP
  • Adenylyl Cyclases