Stanojević Stanislava, Kustrimović Natasa, Mitić Katarina, Miletić Tatjana, Vujić Vesna, Kovacević-Jovanović Vesna, Dimitrijević Mirjana
Institute of Virology, Vaccines and Sera Torlak, Immunology Research Center Branislav Janković, Belgrade, Serbia.
Neuroimmunomodulation. 2008;15(2):108-16. doi: 10.1159/000148193. Epub 2008 Aug 5.
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.
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.
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.
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.
鉴于应激经历可改变对随后应激暴露的反应，我们测试了应激介质皮质酮和阿片肽β-内啡肽对从对照大鼠以及24小时前遭受电尾休克应激（ES）或应激目睹程序（SW）的大鼠分离出的巨噬细胞功能的体外影响。
从黑褐家鼠（DA）品系的对照和应激大鼠分离出的腹腔巨噬细胞，在体外用皮质酮或β-内啡肽处理，并测试其黏附、吞噬作用和过氧化氢释放情况。
ES降低了黏附，SW降低了吞噬作用。在遭受ES和SW的大鼠中，皮质酮对吞噬作用的抑制作用消失，而在遭受SW的大鼠中未观察到β-内啡肽对黏附的抑制作用。在本试验中，ES和SW既未直接也未通过改变巨噬细胞对皮质酮和β-内啡肽的反应间接影响H₂O₂释放。
在DA大鼠中，巨噬细胞早期激活步骤，即黏附和吞噬作用，比其效应功能（对应于H₂O₂产生）对应激更敏感。我们认为，作用于巨噬细胞的应激神经内分泌介质可能改变了特定的巨噬细胞受体或受体后事件，并改变了它们对体外以皮质酮和β-内啡肽为代表的人工应激源的反应。
