Psychological stress in asthma: repercussions on epigenetics-genetics, immune responses, and pulmonary function in the pediatric population.

In the assessment of childhood asthma, identifying the risk factors associated with exacerbations and broadening this view to understand psychological stress and its repercussions on the inflammatory process of asthma allow a different perspective on this biopsychosocial disease. Psychological stress, as a risk factor for the onset and noncontrol of asthma, has been increasingly evaluated from the perspective of the repercussions on the body of the stimulus generated in the hypothalamic-pituitary axis and adrenal glands, with cortisol release and immune system action. These processes trigger changes in T helper 2 cells, which polarize allergic processes, and dysfunctions in immune tolerance mechanisms, with a decrease in regulatory T cells. Genetic and epigenetic changes in β-adrenergic and glucocorticoid receptors, with decreased response to these drugs, were also identified in studies, in addition to changes in respiratory function patterns, with worsening of obstruction and inflammation identified via decreased forced expiratory volume in one second and increased exhaled inflammatory gases in allergic asthma. Therefore, the present review sought to identify studies on the effect of personal and parental acute or chronic psychological stress, emphasizing the repercussions on genetics, epigenetics, and immune and pulmonary functional and inflammatory responses in the pediatric population.