Affiliations: Faculty of Medicine, Department of Immunology, The University of Manitoba, Winnipeg, MB, Canada | Department of Physiology, Autonomous University of Aguascalientes, Aguascalientes, Mexico | Department of Bioquímica, ESM, IPN, Mexico | Department of Laboratory Medicine, St. Michael's Hospital, University of Toronto, Toronto, Canada
Note: [] Correspondence to: Dr. Istvan Berczi, Department of Immunology, The University of Manitoba Winnipeg, MB R3E0T5, Canada. Tel.: +1 789 3509; Fax: +1 789 3921; E-mail: berczii@ms.umanitoba.ca
Abstract: Hypothalamus-Pituitary – Adrenal, (HPA) axis activation and prolactin (PRL) release was studied in rats having chronic experimental autoimmune encephalitis (EAE). Corticotropin releasing hormone (CRH) did not respond to the inflammatory stimulus, but vasopressin (VP), glucocorticoids (GC) and PRL responded at 15 or 29 days of disease. The responses of corticosterone (COS) and of PRL to inflammation were mediated by VP. VP also controlled cytokine release in rats with adjuvant arthritis (AA). The VP agonist, desmopressin (DP), released GC, PRL and restored EAE reactivity in neurointermediate hypohysectomy (NIL) rats. Thus VP regulates the chronic inflammatory process, which eventually leads to healing and recovery from acute febrile illness. After healing VP remains in control of homeostasis in the host. The effects of anterior-, posterior- and total pituitary hormones were examined on cytokine (interleukins-IL-1, -2, -6, -10, -12 and interferon (IFN)-gamma) release during AA of rats. Hormones amplified or inhibited cytokines, which indicated their biological function in immunoregulation.
