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Clinical depression and regulation of the inflammatory response during acute stress.

机译:临床抑郁症和急性应激过程中的炎症反应调节。

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OBJECTIVE: This study examined whether clinical depression is associated with a differential inflammatory response to an acute bout of psychological stress. METHODS: A total of 72 women participated in the study; half met diagnostic criteria for clinical depression; the others had no history of psychiatric illness. The groups were matched with respect to age and ethnicity. All subjects were exposed to a 17-minute mock-job interview; blood was drawn to assess secretion and regulation of inflammatory molecules. RESULTS: The stressor was associated with feelings of shame and anxiety, a mobilization of monocytes, neutrophils, and C-reactive protein into the circulation, and greater endotoxin-stimulated production of interleukin-6 and tumor necrosis factor-alpha by white blood cells in vitro. Depressed subjects began the session with greater sensitivity to the antiinflammatory properties of glucocorticoids than control subjects. Following exposure to the stressor protocol, however, sensitivity decreased among depressed subjects and increased among controls. This was manifest by disparities in interleukin-6 and tumor necrosis factor-alpha production in the presence of dexamethasone. CONCLUSIONS: These findings suggest that under acutely challenging conditions, depression is associated with greater resistance to molecules that normally terminate the inflammatory cascade. An impaired capacity to regulate inflammation could underlie some of the excess morbidity and mortality that has been associated with depression.
机译:目的:本研究检查了临床抑郁症是否与对急性心理应激的不同炎症反应有关。方法:共有72名妇女参加了研究。一半符合临床抑郁症的诊断标准;其他人没有精神病史。各组在年龄和种族方面都匹配。所有受试者均接受了17分钟的模拟面试;抽取血液以评估炎症分子的分泌和调节。结果:应激源与羞耻感和焦虑感,单核细胞,中性粒细胞和C反应蛋白的动员进入循环以及内毒素刺激白细胞中白细胞介素6和肿瘤坏死因子α的产生有关。体外。与对照组相比,抑郁的受试者对糖皮质激素的抗炎特性具有更高的敏感性。然而,在暴露于应激实验方案后,抑郁症患者的敏感性降低,而对照组患者的敏感性提高。在地塞米松的存在下,白介素-6和肿瘤坏死因子-α产生的差异表明了这一点。结论:这些发现表明,在急性挑战性条件下,抑郁症与对通常终止炎症级联反应的分子具有更大的抵抗力有关。调节炎症的能力受损可能是与抑郁症相关的一些额外发病率和死亡率的基础。

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