Infection resistance is enhanced by acute stress. Chronic stress alters this mechanism, reducing the body's capacity for a robust immune response and leading to an increase in morbidity. While chronic stress impairs this mechanism, acute stress likely induces an increase in chemotaxis and adhesion molecules expression through a sympatho–adrenergically mediated mechanism, thereby promoting immune cell migration to infection and/or inflammation sites. Extended distressing circumstances decline NK cytotoxic limit. The increase in cytokine production by macrophages is mediated by a substance called P in stressful conditions. Through a beta2–adrenergically mediated process, acute stress increases T cell mobilization, whereas chronic stress reduces it. The immune system's ability to produce antibodies in response to a vaccine is impaired by psychological stress, making the organism more susceptible to infections.
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Journal of Metabolic Syndrome received 48 citations as per Google Scholar report