Figure 1: The mechanism of chronic stress acting on inflammatory cytokines. The chronic stress activates the (i) HPA and (ii) SAM axis and, respectively, secretes glucocorticoids and catecholamines hormones, which in turn act on the receptors on the surface or in the cytoplasm of the immune cells, (iii) and, meanwhile, motor vagus fiber also secretes catecholamines and ultimately inhibits the proinflammatory cytokines while promoting the anti-inflammatory cytokines. (iv) Both the glucocorticoids and catecholamines promote the Th1 to Th2 shift, including inhibiting the IL-12 secretion and further boosting the shift. (v) At the cellular level, the signal transduction level, stress hormones inhibit the inflammation related pathways, including NF-κB, and further inhibit the proinflammatory cytokines secretion.