Respuesta inmunológica frente al estrés y estado de depresión

Abstract

Chronic oxidative stress in cells generates reactive species that cause their apoptosis or necrosis, which marks a starting point for the inflammation process through the activation of the complement system and the release of inflammatory mediators, especially of cytokines, producing in turn the stimulation of the HPA axis, in charge of the final release of cortisol, to counteract the increase of said inflammation markers as a negative feedback, in this way an adequate balance is maintained. The problem lies when stress is prolonged and there is an increase in inflammatory proteins and hormones that have been associated in various studies with a mood condition classified as depression. For this reason, the research objective is to analyze the damage to the immune response as a product of oxidative stress in patients with depression, through the bibliographic review of scientific articles in databases and national and international repositories, to understand the process at a global level. cell phone. When prolonged stressful conditions occur, macrophage activation is induced and the presence of pro-inflammatory mediators and cortisol increases through CRF activation, it also decreases the ability of neutrophils to perceive chemotactic stimuli, reduces phagocytosis, directly affects organs such as the thymus and the spleen, thus negatively influencing the functioning of the innate immune system and the adaptive response, both cellular and humoral.