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• W2021673485 startingPage "372" @default.
• W2021673485 abstract "ACTH is the primary regulator of adrenal function during acute stress. However, during chronic inflammatory stress additional factors play a major role in the regulation of adrenal secretion. Many cytokines circulate in the blood and are synthesized and released from adrenal tissue. Furthermore, these peptides modify adrenal function. Recently, interleukin-4 (IL-4) was demonstrated to be released from a human adrenal tumor cell line. Therefore, we hypothesized that normal bovine adrenocortical cells could express IL-4 and that this cytokine may modify adrenal function. We determined that IL-4 and IL-4 receptors (IL-4R) are expressed in the bovine adrenal cortex whereas the expression of IL-4 and IL-4R in the adrenal medulla was not apparent. Exposure of dispersed bovine adrenocortical cells isolated from the zona fasciculate to IL-4 did not modify basal release of cortisol. However, the ACTH-stimulated release of cortisol from the bovine adrenal cells was augmented by IL-4. IL-4 exposure had no affect on adrenal androgen release from bovine zona reticularis cells, but IL-4 inhibited the ACTH-stimulated release of adrenal androgens from these cells. The effects of IL-4 on ACTH-stimulated cortisol and adrenal androgen release were dependent upon the IL-4 incubation interval and the IL-4 concentration. Because communication between the immune and endocrine systems is important in inflammatory conditions, IL-4 may play a role in coordinating the adrenal response to inflammatory stress." @default.
• W2021673485 created "2016-06-24" @default.
• W2021673485 creator A5034833354 @default.
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• W2021673485 date "2008-05-01" @default.
• W2021673485 modified "2023-10-06" @default.
• W2021673485 title "Interleukin-4 increases cortisol release and decreases adrenal androgen release from bovine adrenal cells" @default.
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• W2021673485 doi "https://doi.org/10.1016/j.domaniend.2007.10.004" @default.
• W2021673485 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18055157" @default.
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