Stress, cytokine patterns and susceptibility to disease.
Recent evidence indicates that glucocorticoids and catecholamines, the end-products of the stress system, and histamine, a product of activated mast cells, might selectively suppress cellular immunity, and favour humoral immune responses. This is mediated by a differential effect of stress hormones and histamine, on T helper 1 (Th1)/Th2 patterns and type 1/type 2-cytokine production. Thus, systemically, stress might induce a Th2 shift, while, locally, under certain conditions, it might induce pro-inflammatory activities through neural activation of the peripheral corticotropin-releasing factor-mast cell-histamine axis. Through the above mechanisms, stress may influence the onset and/or course of infectious, autoimmune/inflammatory, allergic and neoplastic diseases.
Elenkov
I J
IJ
Pediatric Endocrinology Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Chrousos
G P
GP
D000818:Animals; D003346:Corticotropin-Releasing Hormone / Q000502:physiology; D016207:Cytokines / Q000378:metabolism* / Q000502:physiology; D004198:Disease Susceptibility / Q000209:etiology*; D006632:Histamine / Q000502:physiology; D006801:Humans; D007107:Immune System / Q000502:physiology; D007109:Immunity; D008407:Mast Cells / Q000502:physiology; D013312:Stress, Physiological / Q000150:complications* / Q000276:immunology / Q000378:metabolism*
D016207:Cytokines; D006632:Histamine; D003346:Corticotropin-Releasing Hormone