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Willenberg, H.S.* ; Päth, G.* ; Vögeli, T.A.* ; Scherbaum, W.A.* ; Bornstein, S.R.*

Role of interleukin-6 in stress response in normal and tumorous adrenal cells and during chronic inflammation.

Ann. NY Acad. Sci. 966, 304-314 (2002)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Interleukin-6 (IL-6) is the end-product of a cytokine signaling cascade and is secreted by specialized immune cells during inflammation. It has a great influence on many functions, including differentiation, stimulation, and activation of immune cells, or other cells of neuroendocrine origin. Thus, IL-6 serves as a key messenger in its communication with the neuroendocrine system, and serves as a potent activator of the hypothalamic-pituitary-adrenal axis at all levels. Changes in the levels of expression of this cytokine and its receptor have been observed during chronic inflammatory disease, and have been associated with tumorigenesis. Therefore, we studied the effect of IL-6 on normal and adenomatous human adrenal cells in vitro. The expression of IL-6 receptor mRNA was quantified within the same tissue. IL-6 potently stimulated cortisol secretion from dispersed normal human adrenal cells. We found immunoreactivity for the IL-6 receptor on cultured cells and paraffin-embedded sections of adrenal tissues. Further, there was a more pronounced expression of IL-6 mRNA in adrenal adenomas of patients with Cushing's syndrome, compared to normal human adrenals. Despite this fact, the sensitivity of cells of adenomatous adrenal glands to IL-6 was significantly decreased relative to cells from normal controls. These results were confirmed employing the permanent adrenocortical cancer cell line model NCI-H295. We infer that the loss of responsivity of tumorous adrenal cells to IL-6, and in part corticotropin, is an important step in the process of adrenal tumorigenesis by which regulation by differentiating proteins is bypassed.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Sprache englisch
Veröffentlichungsjahr 2002
HGF-Berichtsjahr 0
ISSN (print) / ISBN 0077-8923
e-ISSN 1749-6632
Quellenangaben Band: 966, Heft: , Seiten: 304-314 Artikelnummer: , Supplement: ,
Verlag New York Academy of Sciences
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Pancreatic Islet Research (IPI)
PubMed ID 12114287
Erfassungsdatum 2002-12-31