Possible Mechanisms Responsible for Stress Predisposition to Cancer or to Autoimmune Diseases
Paolo Lissoni*, Giusy Messina, Roberto Trampetti, Andrea Sassola, Enrica Porta, Giorgio Porro and Giuseppe Di Fede
Institute of Biological Medicine, Milan, Italy.
Today it is known that the enhanced brain opioid system activity represent the major neurochemical variation occurring in stress conditions. Moreover, it has been shown that a chronic opioid hyperactivation may suppress the anticancer immunity, and promote cancer development. On the contrary, the influence of stress on the autoimmune processes is more complex, since the mu-opioid agonists may stimulate both TGF-beta and IL-17 secretion, which respectively may counteract or promote the onset of the autoimmune diseases. The in vivo preferential effects of opioids on TGF- beta or IL-17 secretions could depend on the functional status of brain cannabinoid system, which has been found to inhibit IL-17 secretion. Then, the neurochemical corrections of the major stress-related neuroendocrine and cytokine alterations could constitute a new physiological approach in the treatment of stress-related disorders.
It is known that stress may predispose to both cancer and autoimmune diseases [1-3]. Then, the physiopathological question is to establish whether the promoting influence of stress on the development both cancer and autoimmune diseases, which are characterized by the opposite immune reactivity, may depend on the type of stress or on the different immunobiological response. Moreover, despite the complexity of its mechanisms, it has been proven that stress is mainly characterized by en enhanced brain opioid system activity, since it has been demonstrated that the concomitant administration of an opioid antagonist, such as naloxone o naltrexone (NTX), may abrogate stress-induced immune alterations . Moreover, stress has appeared to be characterized by an enhanced secretion of vasopressin, the so called Antidiuretic Hormone (ADH), by the neurohypophysis, as well as by an increased CRH production at hypothalamic level, with a following activation of the Hypothalamic-Pituitary- Adrenal (HPA) axis and the sympathetic system [5,6]. The mu-opioid agonists, such as beta-endorphin and morphine, have been proven to induce immunosuppression by inhibiting TH1 lymphocyte and dendritic cell functions and by stimulating regulatory T lymphocyte (T reg) system [7,8], with a consequent decreased secretion of IL-2 and IL- 12 in association with an enhanced production of TGF-beta . Being IL-2 and IL-12 the main antitumor cytokines in humans [9,10], and TGF-beta the main endogenous
*Corresponding Author: Paolo Lissoni, Institute of Biological Medicine, Milan, Italy,
Published Date: 07-2020
Copyright© 2020 Paolo Lissoni et al., Journal Of Clinical Neurology, Neurosurgery And Spine. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Citation for this article: Paolo Lissoni, Giusy Messina, Roberto Trampetti, Andrea Sassola, Enrica Porta, Giorgio Porro and Giuseppe Di Fede. Possible Mechanisms Responsible for Stress Predisposition to Cancer or to Autoimmune Diseases. Journal Of Clinical Neurology, Neurosurgery And Spine. 2020; 3(1):124