The effects of corticosterone and beta-endorphin on adherence, phagocytosis and hydrogen peroxide production of macrophages isolated from Dark Agouti rats exposed to acute stress

Abstract

Background: Given that stressful experiences can change the reaction to a subsequent exposure to stress, we tested the in vitro effects of the stress mediator corticosterone and the opioid peptide beta-endorphin on the function of macrophages isolated from control rats and from rats exposed to electric tail shock stress (ES) or a stress-witnessing procedure (SW) 24 h earlier. Methods: Peritoneal macrophages isolated from control and stressed rats of the Dark Agouti (DA) strain were treated in vitro with corticosterone or beta-endorphin and tested for adherence, phagocytosis and hydrogen peroxide release. Results: ES diminished adherence and SW decreased phagocytosis. The suppressive effect of corticosterone on phagocytosis was absent in rats exposed to ES and SW, while the suppressive effect of beta-endorphin on adherence was not observed in rats exposed to SW. ES and SW did not affect H2O2 release, neither directly nor indirectly by changing macrophage response to corticosterone and beta-endorphin in this test. Conclusions: In DA rats early macrophage activation steps, i.e. adherence and phagocytosis, were more sensitive to stress than their effector function, corresponding to H2O2 production. We suggest that neuroendocrine mediators of stress that converge on macrophages might have changed specific macrophage receptors or postreceptor events and alter their response to artificial stressors, represented by corticosterone and beta-endorphin in vitro. Copyright (C) 2008 S. Karger AG, Basel.