Ali Nida, Strahler Jana, Nater Urs M
Department for Clinical and Health Psychology, University of Vienna, Vienna, Austria.
Department of Sport and Sport Science, University of Freiburg, Freiburg, Germany.
Brain Behav Immun. 2025 Jan;123:707-716. doi: 10.1016/j.bbi.2024.10.013. Epub 2024 Oct 13.
Fatigue is a common and debilitating symptom of a broad spectrum of diseases. Previous research has shown that individuals suffering from chronic forms of fatigue experience significantly more stress compared to healthy individuals, suggesting that stress is a potential pathophysiological factor in the onset and maintenance of chronic fatigue. Individually, chronic experiences of fatigue and stress have been associated with disruptions in adaptive immunity. However, how chronic fatigue and chronic stress together affect immune regulation is not fully understood. Here, we investigated the unique and combined contribution of chronic fatigue and chronic stress on immune cell redistribution in response to, and recovery from, acute psychosocial stress. Eighty women with high or low levels of chronic fatigue and varying levels of chronic stress were exposed to a psychosocial laboratory stressor. Blood samples were collected 10 min before and then at 10, 40, and 100 min after the end of stress. The main lymphocyte subpopulations (CD3+, CD3 + CD4+, CD3 + CD8+, CD16 + CD56+, and CD19 + cells) were enumerated via flow cytometry. Acute stress resulted in an increase in CD8 + and CD16+/CD56 + cells, a decline in CD4 + cells, and no effects on CD19 + B lymphocytes. Importantly, the magnitude of immune cell redistribution during stress reactivity (CD3+, CD4+, CD16+/CD56 + ) and recovery (CD3 + ) was contingent on fatigue and chronic stress levels of individuals. Notably, in contrast to low-fatigued individuals, who showed steeper changes in cell populations, increasing levels of chronic stress did not impact immune cell migration responses in high-fatigued individuals. Our findings demonstrate the compounded blunting effects of fatigue and chronic stress on adaptive immune functioning, highlighting a potential pathway for vulnerability and detrimental effects on long-term health.
疲劳是多种疾病常见且使人衰弱的症状。先前的研究表明，与健康个体相比，患有慢性疲劳的个体经历的压力要大得多，这表明压力是慢性疲劳发生和维持的潜在病理生理因素。就个体而言，疲劳和压力的长期经历都与适应性免疫的破坏有关。然而，慢性疲劳和慢性压力共同如何影响免疫调节尚未完全了解。在此，我们研究了慢性疲劳和慢性压力对免疫细胞重新分布的独特和综合作用，这种重新分布是对急性心理社会压力的反应以及从该压力中恢复的过程。80名慢性疲劳水平高或低且慢性压力水平不同的女性暴露于心理社会实验室应激源。在压力结束前10分钟以及结束后10、40和100分钟采集血样。通过流式细胞术对主要淋巴细胞亚群（CD3 +、CD3 + CD4 +、CD3 + CD8 +、CD16 + CD56 +和CD19 +细胞）进行计数。急性应激导致CD8 +和CD16 + / CD56 +细胞增加，CD4 +细胞减少，对CD19 + B淋巴细胞无影响。重要的是，应激反应（CD3 +、CD4 +、CD16 + / CD56 +）和恢复（CD3 +）过程中免疫细胞重新分布的程度取决于个体的疲劳和慢性压力水平。值得注意的是，与低疲劳个体相比，低疲劳个体的细胞群体变化更明显，而慢性压力水平的增加并未影响高疲劳个体的免疫细胞迁移反应。我们的研究结果证明了疲劳和慢性压力对适应性免疫功能的复合钝化作用，突出了对长期健康产生易感性和有害影响的潜在途径。
