title: Cortisol inhibits apoptosis in carp neutrophilic granulocytes.
abstract: The direct effect of cortisol treatment on carp neutrophil viability was examined in vitro. Cortisol treatment caused an inhibition of neutrophil apoptosis. The effect was blocked by glucocorticoid receptor blocker RU486, showing that rescue from apoptosis was receptor mediated. Using binding studies with radioactive cortisol, a single class of glucocorticoid receptors was detected with high affinity (Kd = 2.6 nM) and low capacity (497 receptors/cell) for cortisol binding. Both in vitro and in vivo cortisol treatment did not affect neutrophil respiratory burst activity. These data indicate that cortisol can augment the supply of functional neutrophilic granulocytes in conditions of acute stress, which may be essential for survival, since phagocytes form the first line of defence against micro-organisms.
authors.affiliation: Department of Animal Sciences, Agricultural University, Wageningen, The Netherlands.
authors.forename: F A
authors.initials: FA
authors.lastname: Weyts
authors.forename: G
authors.initials: G
authors.lastname: Flik
authors.forename: B M
authors.initials: BM
authors.lastname: Verburg-van Kemenade
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002347:Carps / Q000097:blood*; D005260:Female; D006098:Granulocytes / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D006854:Hydrocortisone / Q000378:metabolism* / Q000494:pharmacology; D008297:Male; D009504:Neutrophils / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D011965:Receptors, Glucocorticoid / Q000378:metabolism; D016897:Respiratory Burst
chemical_list: D011965:Receptors, Glucocorticoid; D006854:Hydrocortisone