The influence of stress and methionine-enkephalin on macrophage functions in two inbred rat strains

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• 作者：Stanislava Stanojevi&#x107 ; Katarina Miti&#x107 ; Vesna Vuji&#x107 ; Vesna Kovač ; evi&#x107 ; -Jovanovi&#x107 ; ; Mirjana Dimitrijevi&#x107
• 关键词：Albino Oxford rats ; Dark Agouti rats ; Electric tail shock stress ; Stress witnessing procedure ; Methionine-enkephalin ; Peritoneal macrophages ; Phagocytosis ; Hydrogen peroxide production
• 刊名：Life Sciences
• 出版年：2007
• 期刊代码：62_00243205
• 类别：imm
• 出版时间：13 February 2007
• 卷：80
• 期：10
• 页码：901-909
• 文件大小：322 K

摘要

The aim of our current study was to investigate the effect of acute exposure to electric tail shock stress (ES) and to a stress witnessing procedure (SW), as models for physical and psychological stress paradigms, respectively, on phagocytosis and H₂O₂ production in peritoneal macrophages isolated from Albino Oxford (AO) and Dark Agouti (DA) rats. In addition, we studied the in vitro effects of methionine-enkephalin (ME) on phagocytosis and H₂O₂ production in peritoneal macrophages isolated from both AO and DA rats that had been exposed to ES and SW procedures. The results showed that peritoneal macrophages isolated from DA rats were less sensitive to the suppressive effects of ES and SW than macrophages isolated from AO rats. In vitro treatment of macrophages isolated from AO rats with ME mimicked to some extent the suppressive effects of ES and SW on phagocytosis and H₂O₂ production and additionally diminished H₂O₂ release in macrophages isolated from AO rats previously exposed to ES or SW. ME did not have any effect on phagocytosis in macrophages isolated from DA rats, but changed H₂O₂ production in a concentration-dependent manner. In macrophages isolated from DA rats previously exposed to stress the effect of ME was dependent on the macrophage function tested and the particular stress paradigm employed. Our results emphasise the fact that both beneficial and detrimental effects of stress on immune system functions could be attributed to the individual variations in the macrophage's response to stress mediators.