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.
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 H(2)O(2) 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 H(2)O(2) 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.
Stanojević
Stanislava
S
Institute of Virology, Vaccines and Sera Torlak, Immunology Research Center Branislav Janković, Belgrade, Serbia. canac@EUnet.yu
Kustrimović
Natasa
N
Mitić
Katarina
K
Miletić
Tatjana
T
Vujić
Vesna
V
Kovacević-Jovanović
Vesna
V
Dimitrijević
Mirjana
M
D000208:Acute Disease / Q000523:psychology; D000818:Animals; D002448:Cell Adhesion / Q000187:drug effects / Q000276:immunology; D002469:Cell Separation; D002478:Cells, Cultured; D002634:Chemotaxis, Leukocyte / Q000187:drug effects / Q000502:physiology; D003345:Corticosterone / Q000494:pharmacology*; D004195:Disease Models, Animal; D004597:Electroshock / Q000009:adverse effects; D006861:Hydrogen Peroxide / Q000378:metabolism; D007107:Immune System / Q000276:immunology* / Q000378:metabolism; D007108:Immune Tolerance / Q000187:drug effects / Q000276:immunology; D007155:Immunologic Factors / Q000494:pharmacology; D007166:Immunosuppressive Agents / Q000494:pharmacology; D017737:Macrophages, Peritoneal / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D008297:Male; D015213:Neuroimmunomodulation / Q000276:immunology; D009490:Neurosecretory Systems / Q000276:immunology; D010587:Phagocytosis / Q000187:drug effects / Q000276:immunology*; D051381:Rats; D013045:Species Specificity; D013315:Stress, Psychological / Q000276:immunology*; D001615:beta-Endorphin / Q000494:pharmacology*
D007155:Immunologic Factors; D007166:Immunosuppressive Agents; D001615:beta-Endorphin; D006861:Hydrogen Peroxide; D003345:Corticosterone