Figure 1.

Stress-induced periphery inflammation and neuroinflammation in stress-related disorders: mechanisms and consequences interaction between the immune system, HPA axis, and sympathetic nervous system. Exposure to traumatic and stressful events in individuals may facilitate increased immune activity in both the periphery and the central nervous system (CNS) by activating the HPA axis and the sympathetic nervous system (SNS). HPA axis activation results in the release of glucocorticoids, which modulate the inflammatory response by suppressing the expression of pro-inflammatory cytokines by immune cells. However, overactivity of the SNS increases the release of pro-inflammatory cytokines. These cytokines access the brain via afferent fibers (e.g., vagus nerve) or through the damaged blood–brain barrier to activate microglia, which in turn contribute to neuroinflammation via secretion of pro-inflammatory cytokines in the brain.