Stress modulates the immune response through the psychoneuroimmunoendocrine pathway and the hypothalamic-pituitary-adrenal axis  via the release of cortisol, norepinephrine, epinephrine and interferon-gamma (IFN-γ) by T lymphocytes. Increased levels of proinflammatory cytokines such as IFN-γ (T helper cell type 1 (Th1) cytokine) and a rapid but tissue-damaging cellular immune response constitute the immune system response . Cortisol and catecholamines decrease the production of tumor necrosis factor-alpha (TNF-α) by antigen-presenting cells and promote Th2 responses via the release of interleukin (IL)10, IL13 and IL4 . This process permits the immune system to halt acute responses but also favors allergic diseases [14, 15]. It has recently been found that epigenetic factors encourage the development of inadequate stress responses, paving the way for a chronic stress response instead of an acute stress response [10, 16, 17].