Depression and immune function - Central pathways to morbidity and mortality
Depression and immune function - Central pathways to morbidity and mortality
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DOI：
10.1016/s0022-3999(02)00309-4
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发表时间：
2002-10-01
影响因子：
4.7
通讯作者：
Glaser, R
中科院分区：
文献类型：
--
作者：
Kiecolt-Glaser, JK;Glaser, R
目的：抑郁症的发病率和死亡率显著增加。在本文中，我们回顾的证据表明，抑郁症有助于疾病和死亡，通过免疫失调。方法：本文综述了最近关于抑郁症对免疫功能的影响以及这些变化对健康的影响的人类研究。结果如下：越来越多的证据表明，抑郁症可以直接刺激促炎细胞因子的产生，这些细胞因子会影响与衰老相关的一系列疾病，包括心血管疾病、骨质疏松症、关节炎、2型糖尿病、某些癌症、牙周病、虚弱和功能衰退。此外，抑郁症可以下调细胞免疫反应;因此，抑郁症可能会促进诸如延长感染和延迟伤口愈合等过程，从而促进持续的促炎细胞因子产生。结论：这些直接和间接的过程对老年人造成了最大的健康风险，他们已经表现出与年龄相关的促炎细胞因子产生增加。因此，衰老与抑郁症相互作用，增加了发病率和死亡率的风险。(C)2002年爱思唯尔科技有限公司All rights reserved.
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.