Acute stress increases resistance to infection. The alteration of this mechanism in chronically stressed people impairs the organism’s ability to mount a strong immune response with a resultant increase in morbidity. Acute stress induces a probable sympatho–adrenergically mediated increase in chemotaxis and adhesion molecules expression, thus promoting immune cells migration to sites of infection and/or inflammation, while chronic stress impairs this mechanism. Protracted stressful conditions decrease NK cytotoxic capacity. There is a substance P, which under stressful circumstances mediates the increase in macrophage cytokine production. Acute stress increases T cell mobilization through a beta2–adrenergically mediated process, which is blunted during chronic stress. Psychological stress impairs the immune system’s ability to produce antibodies in response to a vaccine, thereby making the organism more vulnerable to infections.

Abbreviations: CRH = corticotrophin–releasing hormone; HPA = hypothalamic–pituitary–adrenocortical; IL = interleukin; NE = norepinephrine; NK = natural killer; SAM = sympathetic–adrenal medullary; S–IgA = secretory immunoglobulin A; SNS = sympathetic nervous system; TGF = transforming growth factor; Th = T helper; TNF = tumor necrosis factor