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 β-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 β-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 β-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 β-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 β-endorphin in vitro.