The effect of stress on the defense systems.

TLDR

Substance P mediates increased macrophage cytokine production under stress. Acute stress enhances immune defenses—boosting chemotaxis, T‑cell mobilization, and resistance to infection—whereas chronic stress impairs these mechanisms, reducing NK cytotoxicity, antibody production, and overall immune responsiveness, leading to higher morbidity.

Abstract

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.