Walther Lisa-Marie, Gideon Angelina, Sauter Christine, Leist Marcel, Wirtz Petra H
Biological Work and Health Psychology, University of Konstanz, 78457 Konstanz, Germany.
Centre for the Advanced Study of Collective Behaviour, University of Konstanz, 78457 Konstanz, Germany.
Cells. 2024 Nov 22;13(23):1941. doi: 10.3390/cells13231941.
Psychosocial stress has been proposed to induce a redistribution of immune cells, but a comparison with an active placebo-psychosocial stress control condition is lacking so far. We investigated immune cell redistribution due to psychosocial stress compared to that resulting from an active placebo-psychosocial stress but otherwise identical control condition. Moreover, we tested for mediating effects of endocrine parameters and blood volume changes. The final study sample comprised 64 healthy young men who underwent either a psychosocial stress condition (Trier Social Stress Test; TSST; = 38) or an active placebo-psychosocial stress control condition (PlacTSST; = 26). Immune cell counts and hemoglobin, epinephrine, norepinephrine, ACTH, renin, and aldosterone levels, as well as those of saliva cortisol, were determined before and up to 30 min after the TSST/PlacTSST. The TSST induced greater increases in total leukocyte, monocyte, and lymphocyte levels as compared to the PlacTSST ('s ≤ 0.001), but in not granulocyte counts. Neutrophil granulocyte counts increased in reaction to both the TSST and PlacTSST ('s ≤ 0.001), while eosinophil and basophil granulocyte counts did not. The psychosocial stress-induced increases in immune cell counts from baseline to peak (i.e., +1 min after TSST cessation) were independently mediated by parallel increases in epinephrine (ab's ≤ -0.43; 95% CIs [LLs ≤ -0.66; ULs ≤ -0.09]). Subsequent decreases in immune cell counts from +1 min to +10 min after psychosocial stress cessation were mediated by parallel epinephrine, renin, and blood volume decreases (ab's ≥ 0.17; 95% CIs [LLs ≥ 0.02; ULs ≥ 0.35]). Our findings indicate that psychosocial stress specifically induces immune cell count increases in most leukocyte subpopulations that are not secondary to the physical or cognitive demands of the stress task. Increases in the number of circulating neutrophil granulocytes, however, are not psychosocial stress-specific and even occur in situations with a low probability of threat or harm. Our findings point to a major role of epinephrine in mediating stress-induced immune cell count increases and of epinephrine, renin, and blood volume changes in mediating subsequent immune cell count decreases from +1 min to +10 min after psychosocial stress cessation.
心理社会应激已被认为可诱导免疫细胞重新分布，但目前尚缺乏与主动安慰剂 - 心理社会应激对照条件的比较。我们研究了心理社会应激引起的免疫细胞重新分布，并与主动安慰剂 - 心理社会应激但其他方面相同的对照条件所导致的情况进行比较。此外，我们还测试了内分泌参数和血容量变化的中介作用。最终研究样本包括64名健康年轻男性，他们分别接受了心理社会应激条件（特里尔社会应激测试；TSST；n = 38）或主动安慰剂 - 心理社会应激对照条件（PlacTSST；n = 26）。在TSST/PlacTSST之前及之后长达30分钟内，测定免疫细胞计数以及血红蛋白、肾上腺素、去甲肾上腺素、促肾上腺皮质激素、肾素和醛固酮水平，还有唾液皮质醇水平。与PlacTSST相比，TSST诱导总白细胞、单核细胞和淋巴细胞水平有更大幅度升高（p值≤0.001），但粒细胞计数无变化。中性粒细胞计数在TSST和PlacTSST作用下均升高（p值≤0.001），而嗜酸性粒细胞和嗜碱性粒细胞计数未升高。心理社会应激诱导的免疫细胞计数从基线到峰值（即TSST停止后 +1分钟）的增加，独立地由肾上腺素的平行增加介导（间接效应ab's≤ -0.43；95%置信区间[下限≤ -0.66；上限≤ -0.09]）。心理社会应激停止后从 +1分钟到 +10分钟免疫细胞计数的后续减少，由肾上腺素、肾素和血容量的平行减少介导（间接效应ab's≥0.17；95%置信区间[下限≥0.02；上限≥0.35]）。我们的研究结果表明，心理社会应激特异性地诱导大多数白细胞亚群的免疫细胞计数增加，这并非应激任务的身体或认知需求所继发。然而，循环中性粒细胞数量的增加并非心理社会应激所特有，甚至在威胁或伤害可能性较低的情况下也会发生。我们的研究结果表明，肾上腺素在介导应激诱导的免疫细胞计数增加中起主要作用，而肾上腺素、肾素和血容量变化在介导心理社会应激停止后从 +1分钟到 +10分钟的后续免疫细胞计数减少中起作用。
