Stress, neutrophils, and immunity: a dynamic interplay

Abstract

Neutrophils, the most abundant type of white blood cells, are pivotal players in the innate immune system, responsible for rapid responses to infection and tissue damage. They engage in various defensive activities, including phagocytosis, degranulation, and the formation of neutrophil extracellular traps (NETs). Stress, encompassing both physiological and psychological forms, significantly influences the immune system, notably impacting neutrophil function. This review delves into the intricate interplay between stress, neutrophils, and immunity, underscoring how stress modulates neutrophil activity and the broader implications for immune health. The body's response to stress involves the activation of the hypothalamic-pituitary-adrenal (HPA) axis and the subsequent release of stress hormones such as cortisol and adrenaline. These hormones can enhance or suppress immune functions, depending on the nature and duration of the stress. Acute stress may temporarily boost neutrophil activity, enhancing the body's immediate defense mechanisms. In contrast, chronic stress typically results in immunosuppression, adversely affecting neutrophil functions and increasing vulnerability to infections and inflammatory diseases. The mechanisms through which stress affects neutrophils include hormonal regulation, neuroimmune interactions, and alterations in the production of inflammatory mediators. The dynamic relationship between stress and neutrophils has significant health implications. While acute stress can enhance immune defenses, chronic stress contributes to a range of health issues, including increased infection risk, autoimmune disorders, and chronic inflammatory conditions such as cardiovascular disease and cancer.