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Psychological stress, immune response, and atherosclerosis

H Gu, C Tang... - Atherosclerosis, 2012 - Elsevier Abstract 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 ...

Fig. 1. Psychological stressors result in the activation of the HPA axis and the SAM axis. The production of adrenocorticotropic hormone by the pituitary gland results in the production of glucocorticoid hormones. The SAM axis can be activated by stimulation of the adrenal medulla to produce the catecholamines epinephrine and NE. Glucocorticoid hormones and catecholamines are able to modulate the immune response via receptors expressed on the immune cells. This regulation might be either attenuative or intensifying, depending on the costimulus. In addition, psychological stressors also increase the expression of Toll-like receptor 4 (TLR4) in immune cells, which increase the sensitivity to internal stressors, including pathogen associated molecular patterns (PAM Ps) and damage-associated molecular patterns (DAM Ps). Pathway involves in stress activation of either nuclear factor-κB (NF-κB) or mitogen activated protein kinases (MAP Ks) pathway signaling. These would increase levels of pro-inflammatory cytokines, such as interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-6. However, these cytokines might promote production of each other, and change the level of stress hormone. My D88, myeloid differentiation factor-88; TRIF, TIR domain-containing adapter protein inducing IFN-β; β-AR, beta-adrenergic receptor; GR, glucocorticoid receptor.