Regulation of Steroidogenesis in Reproductive, Adrenal and Neural Tissues by Cytokines

Steroid hormones have a large number of functions in the organism, including the regulation of stress response, the electrolytic balance, and reproduction. The synthesis of these hormones is mediated by a series of enzymes, which produce glucocorticoids, mineralocorticoids, progestins, androgens and estrogens using cholesterol as the metabolic main precursor. In this general way, steroid synthesis regulation depends on signals constituted by proteinic hormones (corticotrophin releasing hormone (CRH) and adrenocorticotropic hormone (ACTH) in the case of glucocorticoids, and (gonadotropin releasing hormone (GnRH), luteinizing hormone (LH), and follicle stimulating hormone (FSH) in the case of sex hormones, which bind to their specific receptors. However, this is not the only regulatory mechanism of the steroidogenic pathway. It has been observed that the neuroendocrine axes also interact with the immune system. Thus, this bidirectional communication between these two systems has currently been accepted. Steroids can regulate some functions of the immune system, and, viceversa, molecules secreted by the immune system modulate steroid synthesis. This is the case of cytokines. These molecules participate in the immune response and are secreted by different immunological cells. Their functions include activation and proliferation of the immune cells as well as mediation of the inflammatory process. Gonadal and adrenal steroidogenesis regulation by direct or bidirectional communication between the immunologic and neuroendocrine systems has been well established. Cytokines play a key role in this interaction, and their production is influenced by the direct action of hormones and neurohormones on immune system cells. The action of some of the main cytokines produced by the immunologic system on the regulation of gonadal (ovarian and testicular), adrenal and neural steroidogenesis is summarized in this review.