Depression and immune function - Central pathways to morbidity and mortality

被引:420
作者
Kiecolt-Glaser, JK
Glaser, R
机构
[1] Ohio State Univ, Coll Med, Dept Psychiat, Columbus, OH 43210 USA
[2] Ohio State Univ, Coll Med, Dept Mol Virol Immunol & Med Genet, Columbus, OH 43210 USA
关键词
proinflammatory cytokines; interleukin; 6; psychoneuroimmunology; stress;
D O I
10.1016/S0022-3999(02)00309-4
中图分类号
R749 [精神病学];
学科分类号
100205 ;
摘要
Objective: The increased morbidity and mortality associated with depression is substantial. In this paper, we review evidence suggesting that depression contributes to disease and death through immune dysregulation. Method: This review focuses on recent human studies addressing the impact of depression on immune function, and the health consequences of those changes. Results: There is growing evidence that depression can directly stimulate the production of proinflammatory cytokines that influence a spectrum of conditions associated with aging, including cardiovascular disease, osteoporosis, arthritis, type 2 diabetes, certain cancers, periodontal disease, frailty, and functional decline. Additionally, depression can down-regulate the cellular immune response; as a consequence, processes such as prolonged infection and delayed wound healing that fuel sustained proinflammatory cytokine production may be promoted by depression. Conclusions: These direct and indirect processes pose the greatest health risks for older adults who already show age-related increases in proinflammatory cytokine production. Thus, aging interacts with depression to enhance risks for morbidity and mortality. (C) 2002 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:873 / 876
页数:4
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