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Developmental Endocrinology Branch, National Institute of Child Health and Human Development (R. W. W., R.A.K.) Health, Bethesda, Maryland 20892
The Surgery Branch, National Cancer Institute (W.M.L.) Bethesda, Maryland 20892
The Laboratory Microbiology and Immunology, National Institute of Dental Research (L.M. W.), National Institutes of Health Bethesda, Maryland 20892
Address all correspondence and requests for reprints to: Randall W. Whitcomb, M.D., Building 10, Room 10N262, National Institutes of Health, Bethesda, Maryland 20892.
Studies using cultured human adrenocortical cells were performed to determine if the immune modulation of glucocorticoid production previously described in animal studies also occurs in humans. Human monocytes significantly increased (P < 0.001) cortisol production from adrenocortical cells after 24, 48, and 72 h of culture. This stimulation was not CRH dependent, and the presence of CRH alone did not augment cortisol production. The active factor was soluble, since supernatants of monocyte cultures stimulated cortisol production by adrenocortical cells; ACTH levels in these supernatants were undetectable by RIA. While interleukin-1 also stimulated cortisol production by adrenal cells, the degree of stimulation was only 30% of that in the monocyte experiments. In contrast to previous animal studies, we found that human monocytes stimulate cortisol production by human adrenocortical cells by a factor that is neither CRH dependent nor mediated by immunoreactive ACTH-(l–24) or ACTH-(l–39).
Received June 10, 1987.
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