Psychological stress, immune response, and atherosclerosis.
It is well known that psychological stress is associated with increased atherosclerosis. This response is mainly mediated by altered immune reactions due to either activation or depression of the hypothalamic-pituitary-adrenal (HPA) regulatory feed back mechanisms that influence both the vascular endothelium function and the recruitment of circulating monocytes and their conversion to foam cells. Although the detailed mechanisms behind these processes are not well understood, it has been assumed that expression of pro- and anti-inflammatory cytokines by stress hormones, such as catecholamines and corticosteroids, maybe involved. In this review, we focus on evidences that various immunological factors are transformed under prolonged psychological stress by causing vascular low-grade inflammation. A better understanding of the bidirectional communication between the neuroendocrine and immune systems may contribute to new treatment strategies.
Department of Physiology, University of South China, Hengyang, China. ghf513@sina.com
Hong-feng
HF
Gu
Chao-ke
CK
Tang
Yong-zong
YZ
Yang
D000818:Animals; D050197:Atherosclerosis / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology / Q000523:psychology; D016207:Cytokines / Q000378:metabolism; D004730:Endothelium, Vascular / Q000276:immunology / Q000503:physiopathology; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000276:immunology* / Q000503:physiopathology; D018836:Inflammation Mediators / Q000378:metabolism; D010913:Pituitary-Adrenal System / Q000276:immunology* / Q000503:physiopathology; D011379:Prognosis; D018570:Risk Assessment; D012307:Risk Factors; D015398:Signal Transduction; D013315:Stress, Psychological / Q000150:complications* / Q000276:immunology / Q000503:physiopathology
D016207:Cytokines; D018836:Inflammation Mediators