Institute of Psychology, University of Duisburg-Essen, Berliner Platz 6-8, 45127 Essen, Germany.
Biol Psychol. 2013 Feb;92(2):403-9. doi: 10.1016/j.biopsycho.2012.12.003. Epub 2012 Dec 16.
According to the effort-reward-imbalance (ERI) model, a lack of reciprocity between costs and gains at work increases the risk for adverse health outcomes. Inflammation has been shown to play a crucial role in a variety of stress-related diseases and alterations in immune system glucocorticoid sensitivity may help to explain the increased risk for cardiovascular disease (CVD) and depression related to chronic work stress.
Changes in lipopolysaccharide (LPS)-induced interleukin (IL)-6 production and inhibition of IL-6 production by dexamethasone in reaction to the Trier Social Stress Test (TSST) were assessed in forty-six healthy school teachers to test whether chronic work stress is accompanied by alterations in inflammatory activity and glucocorticoid sensitivity of the innate immune system.
High ERI was associated with an increase in pro-inflammatory potential, reflected in elevated IL-6 production before and after stress and with a lower capacity of dexamethasone to suppress IL-6 production in vitro over all measurement time points. ERI was not associated with stress-related changes in GC sensitivity.
The present findings suggest a less effective anti-inflammatory regulation by glucocorticoids in teachers suffering from chronic work stress.
根据工作投入-回报失衡(ERI)模型,工作中的成本与收益之间缺乏互惠性会增加不良健康结果的风险。炎症已被证明在各种与压力相关的疾病中起着至关重要的作用,而免疫系统糖皮质激素敏感性的改变可能有助于解释与慢性工作压力相关的心血管疾病(CVD)和抑郁风险增加。
为了测试慢性工作压力是否伴随着固有免疫系统炎症活性和糖皮质激素敏感性的改变,我们评估了 46 名健康学校教师在特里尔社会应激测试(TSST)中脂多糖(LPS)诱导的白细胞介素(IL)-6 产生的变化以及地塞米松对 IL-6 产生的抑制作用。
高 ERI 与促炎潜能增加相关,表现为应激前后 IL-6 产生增加,以及地塞米松在所有测量时间点体外抑制 IL-6 产生的能力降低。ERI 与 GC 敏感性的应激相关变化无关。
本研究结果表明,慢性工作压力下的教师糖皮质激素的抗炎调节作用降低。