The fragile mind: early life stress and inflammatory disease.

摘要

Stress is now recognized as a significant contributory factor in the cause and progression of many diseases (1-3). The sympathetic nervous system (SNS) and the hypothalamo-pituitary-adrenocortical (HPA) axis, the principal pathways that respond to stress, exert tonic inhibitory control over the immune system through multiple coordinated networks involving glucocorticoids, catecholamines, neuropeptides, and cytokines (4-6). Stress can result in a resetting of immune responses with consequent impaired ability of the organism to mount an effective defense after onset of infection or chronic inflammatory disease. The exacerbatory effects of stress on many inflammatory diseases are well documented, although the evidence is rather more anecdotal than scientific. Paradoxically, protective effects of stress on inflammation have been reported (7, 8). A major challenge in the field of psychoneuroimmunology lies in defining the highly complex interactions among the SNS, HPA axis, and immune system to elucidate the selective effects of stress on disease processes.