Journal
STRESS-THE INTERNATIONAL JOURNAL ON THE BIOLOGY OF STRESS
Volume 10, Issue 1, Pages 65-73Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/10253890601181289
Keywords
beta-endorphin (BE); corticosterone (CORT); electric tail shock stress (ES); neuropeptide Y (NPY); peritoneal macrophage functions; stress witnessing procedure (SW)
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The objective of the present study was to investigate the effect of acute exposure to electric tail shock stress (ES) and a stress witnessing procedure ( SW), as models for physical and psychological stress paradigms, respectively on adherence, phagocytosis and hydrogen peroxide (H2O2) release from rat peritoneal macrophages. In addition, we studied the in vitro effects of corticosterone (CORT), neuropeptide Y (NPY) and beta-endorphin (BE) on adherence, phagocytosis and H2O2 release from macrophages isolated from control rats and from rats that had been exposed to ES or SW procedures 24 h earlier. ES and SW comparably diminished phagocytosis and H2O2 release, but did not influence macrophage adherence. In vitro treatment with CORT and NPY notably suppressed phagocytosis and potentiated H2O2 release from macrophages. BE suppressed both phagocytosis and H2O2 release from macrophages. Previous exposure to ES and SW altered the responsiveness of the isolated macrophages to their in vitro treatment with mediators of stress, making the cells less sensitive to the influence of CORT and NPY and to a lesser extent to BE. It could be concluded that changes in the local macrophage milieu induced by ES and SW 24 h earlier modify macrophage responses to subsequent in vitro exposure to the stress mimics, CORT, NPY and BE.
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