Acute stress evokes selective mobilization of T cells that differ in chemokine receptor expression: a potential pathway linking immunologic reactivity to cardiovascular disease

被引:72
作者
Bosch, JA
Berntson, GG
Cacioppo, JT
Dhabhar, FS
Marucha, PT
机构
[1] Ohio State Univ, Coll Dent, Periodontol Sect, Columbus, OH 43218 USA
[2] Ohio State Univ, Dept Psychol, Columbus, OH 43210 USA
[3] Univ Chicago, Dept Psychol, Chicago, IL 60637 USA
[4] Ohio State Univ, Inst Behav Med Res, Columbus, OH USA
[5] Ohio State Univ, Coll Dent, Dept Oral Biol, Columbus, OH USA
关键词
cardiovascular disease; acute psychological stressor; psychoneuroimmunology; cardiovascular reactivity; autonomic balance; lymphocyte redistribution; chemokines;
D O I
10.1016/S0889-1591(03)00054-0
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
T lymphocytes and monocytes/macrophages are the most abundant cells found in the atherosclerotic plaque. These cells can migrate towards the activated endothelium. through the local release of chemotactic cytokines, or chemokines. Given the important role of leukocyte migration in atherosclerosis and the role of stress in mediating leukocyte trafficking, the present study examined the effects of an acute stressor on the redistribution of T cells (CD3+) and monocytes that express the chemokine receptors CCR5, CCR6, CXCR1, CXCR2, CXCR3, and CXCR4. Forty-four undergraduate students underwent a public speaking task. The acute stressor induced sympathetic cardiac activation, parasympathetic cardiac withdrawal, lymphocytosis, and monocytosis (all p < .001). Although the total number of T lymphocytes did not change, there was a selective increase in the number of circulating T cells expressing CXCR2, CXCR3, and CCR5. The ligands of these receptors are chemokines known to be secreted by activated endothelial cells. Analyses of individual differences in stress-induced responses demonstrated a positive relationship between sympathetic cardiac reactivity and mobilization of the various T cell subsets (.35 < r < .56; p < .05). For the monocytes, all subpopulations increased in parallel with total monocyte numbers, with no relation to changes in sympathetic cardiac drive. These results indicate that acute stress induces a mobilization of T cells that are primed to respond to inflamed endothelium. Acute stressors may thus promote the recruitment of circulating immune cells into the sub-endothelia, and therefore accelerate atherosclerotic plaque formation and potentially contribute to the complications that follow acute stressful events. This mechanism may help explain the link between stress, reactivity, and cardiovascular disease. (C) 2003 Elsevier Science (USA). All rights reserved.
引用
收藏
页码:251 / 259
页数:9
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