Buske-Kirschbaum A, Kern S, Ebrecht M, Hellhammer D H
Department of Psychobiology, University of Dresden, Dresden, Germany.
Brain Behav Immun. 2007 Jan;21(1):92-9. doi: 10.1016/j.bbi.2006.03.006. Epub 2006 May 22.
Psoriasis (PSO) is a mainly T helper-type 1 (TH(1)) cell mediated chronic inflammatory skin disease characterized by epidermal hyperproliferation and psoriatic plaques. There is ample evidence that stress may trigger psoriatic eruption, however, the underlying mechanisms of stress-induced exacerbation of PSO are poorly understood. The specific goal of the present study was to investigate the impact of acute stress on pathologically relevant immune functions in PSO patients. PSO patients (n=23) and healthy controls (n=25) were exposed to a standardized laboratory stressor ("Trier Social Stress Test", TSST) including a free speech and mental arithmetics in front of an audience. Blood samples were collected 10min before and 1, 10, 20, and 60min after the TSST as well as 24h after the experiment at identical time points under resting conditions. Analyses of leukocyte subsets indicated a significantly increased number of leukocyte subpopulations (lymphocytes, granulocytes, CD3(+), CD8(+), CD16(+)/CD56(+), and CD3(+)/HLA-DR(+)) after the TSST (all p<.01) with no significant between-group differences. However, monocyte number (F(3,120)=2.7; p<.01) and number of CD4(+)cells (F(3,120)=3.09; p<.05) were found to be significantly higher in PSO sufferers than in controls. Moreover, a significant decrease of CD3(+)/CD25(+)cells was observed in the PSO, but not in the control group (F(3,120)=3.46; p<.05). After exposure to the TSST, stimulation of peripheral blood mononuclear cells (PBMCs) with phytohemagglutinin (PHA) resulted in elevated production of IFN-gamma (F(3,126)=6.9; p<.001) and IL-2 (F(3,123)=6.6; p<.001), and moreover, a decreased production of IL-10 (F(3,132)=5.22; p<.01) and IL-4 (F(3,129)=3.9; p<.01). No difference in stress-induced changes of cytokine production to PHA could be identified between the two experimental groups (all p>.05). The present findings suggest that acute psychosocial stress is associated with changes of immune functions known to be involved in PSO which may be one potential explanation of how stress may trigger psoriatic eruption.
银屑病（PSO）是一种主要由辅助性T1型（TH(1)）细胞介导的慢性炎症性皮肤病，其特征为表皮过度增殖和银屑病斑块。有充分证据表明压力可能引发银屑病发作，然而，压力诱发PSO病情加重的潜在机制尚不清楚。本研究的具体目标是调查急性应激对PSO患者病理相关免疫功能的影响。PSO患者（n = 23）和健康对照者（n = 25）暴露于标准化实验室应激源（“特里尔社会应激测试”，TSST），包括在观众面前进行自由演讲和心算。在TSST前10分钟、TSST后1、10、20和60分钟以及实验后24小时的相同时间点在静息条件下采集血样。白细胞亚群分析表明，TSST后白细胞亚群（淋巴细胞、粒细胞、CD3(+)、CD8(+)、CD16(+)/CD56(+)和CD3(+)/HLA-DR(+)）数量显著增加（均p <.01），两组间无显著差异。然而，发现PSO患者的单核细胞数量（F(3,120)=2.7；p <.01）和CD4(+)细胞数量（F(3,120)=3.09；p <.05）显著高于对照组。此外，观察到PSO组CD3(+)/CD25(+)细胞显著减少，而对照组未出现此现象（F(3,120)=3.46；p <.05）。暴露于TSST后，用植物血凝素（PHA）刺激外周血单个核细胞（PBMC）导致IFN-γ（F(3,126)=6.9；p <.001）和IL-2（F(3,123)=6.6；p <.001）产生增加，此外，IL-10（F(3,132)=5.22；p <.01）和IL-4（F(3,129)=3.9；p <.01）产生减少。两个实验组之间在应激诱导的PHA细胞因子产生变化方面未发现差异（均p >.05）。本研究结果表明，急性心理社会应激与已知参与PSO的免疫功能变化相关，这可能是压力引发银屑病发作的一种潜在解释。
