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Social stress induces glucocorticoid resistance in macrophages.

机译:社会压力在巨噬细胞中诱导糖皮质激素抵抗。

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Stress-induced levels of plasma glucocorticoid hormones are known to modulate leukocyte function. These experiments examined the effects of a social stressor on the responsiveness of peripheral immune cells. Male mice experienced six evening cycles of social disruption (SDR), in which an aggressive male intruder was placed into their home cage for 2 h. Although circulating corticosterone was elevated in SDR mice, they had enlarged spleens and increased numbers of splenic leukocytes. Splenocytes from SDR and control mice were cultured with lipopolysaccharide and corticosterone. Cells from SDR mice exhibited decreased sensitivity to the antiproliferative effects of corticosterone, suggesting that the peripheral immune cells were resistant to glucocorticoids. In addition, SDR cells produced more interleukin (IL)-6. To determine which cell population was affected, we used antibody-labeled magnetic beads to deplete splenocyte suspensions of B cells or macrophages. Depletion of macrophages from SDR cultures,but not depletion of B cells, abolished both the corticosterone resistance and enhanced IL-6 secretion. These findings demonstrate that a psychosocial stressor induced glucocorticoid resistance in mouse splenic macrophages.
机译:已知应激诱导的血浆糖皮质激素水平可调节白细胞功能。这些实验检查了社交应激源对外周免疫细胞反应性的影响。雄性小鼠经历了六个晚上的社交破坏(SDR)周期,其中将一个侵略性雄性入侵者放进其家笼中2小时。尽管在SDR小鼠体内循环皮质酮升高,但脾脏增大,脾白细胞增多。用脂多糖和皮质酮培养来自SDR和对照小鼠的脾细胞。来自SDR小鼠的细胞对皮质酮的抗增殖作用表现出降低的敏感性,表明外周免疫细胞对糖皮质激素具有抗性。此外,SDR细胞产生更多的白介素(IL)-6。为了确定受影响的细胞群,我们使用了抗体标记的磁珠来消耗B细胞或巨噬细胞的脾细胞悬液。 SDR培养物中巨噬细胞的消耗,而不是B细胞的消耗,消除了皮质酮耐药性并增强了IL-6分泌。这些发现表明,心理社会应激源在小鼠脾巨噬细胞中诱导了糖皮质激素抵抗。

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