Betamethasone modulates the biological function of human polymorphonuclear leukocytes.
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).
D000262:Adenylyl Cyclases / Q000378:metabolism; D001623:Betamethasone / Q000494:pharmacology*; D000242:Cyclic AMP / Q000378:metabolism; D005089:Exocytosis / Q000187:drug effects; D006801:Humans; D008247:Lysosomes / Q000201:enzymology; D009504:Neutrophils / Q000187:drug effects* / Q000378:metabolism
D001623:Betamethasone; D000242:Cyclic AMP; D000262:Adenylyl Cyclases