β-endorphin secretion by human peripheral blood mononuclear cells: Regulation by glucocorticoids

Corticotropin-releasing factor (CRF), a 41-aminoacid neuropeptide, can induce lymphocytes to production of β-endorphin (βE). Furthermore, the neuropeptide Arginine-Vasopressin (AVP) can enhance CRF-induced production of βE. We have demonstrated that CRF acts by stimulating monocytes to production of the cytokine Interleukin-1 (IL-1). IL-1 can in its turn activate the lymphocytes to secretion of βE. Here we demonstrate that the glucocorticoid analogue dexamethasone is capable of modulating CRF-induced βE secretion by lymphocytes. It appeared that dexamethasone can inhibit secretion of lymphocyte-derived βE. The mechanism by which dexamethasone exerts its inhibitory activity is by blocking CRF-induced production of IL-1, thereby preventing induction of βE secretion by B cells. These results support the concept that peptide hormones and glucocorticoids are mediating a reciprocal modulation of neuroendocrine and immunological activities.