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Research Article Free access | 10.1172/JCI115668

17 beta-estradiol inhibits interleukin-6 production by bone marrow-derived stromal cells and osteoblasts in vitro: a potential mechanism for the antiosteoporotic effect of estrogens.

G Girasole, R L Jilka, G Passeri, S Boswell, G Boder, D C Williams, and S C Manolagas

Section of Endocrinology and Metabolism, Veteran's Administration Medical Center, Indianapolis, Indiana 46202.

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Section of Endocrinology and Metabolism, Veteran's Administration Medical Center, Indianapolis, Indiana 46202.

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Section of Endocrinology and Metabolism, Veteran's Administration Medical Center, Indianapolis, Indiana 46202.

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Section of Endocrinology and Metabolism, Veteran's Administration Medical Center, Indianapolis, Indiana 46202.

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Section of Endocrinology and Metabolism, Veteran's Administration Medical Center, Indianapolis, Indiana 46202.

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Section of Endocrinology and Metabolism, Veteran's Administration Medical Center, Indianapolis, Indiana 46202.

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Section of Endocrinology and Metabolism, Veteran's Administration Medical Center, Indianapolis, Indiana 46202.

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Published March 1, 1992 - More info

Published in Volume 89, Issue 3 on March 1, 1992
J Clin Invest. 1992;89(3):883–891. https://doi.org/10.1172/JCI115668.
© 1992 The American Society for Clinical Investigation
Published March 1, 1992 - Version history
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Abstract

The effect of 17 beta-estradiol on interleukin-6 (IL-6) synthesis was examined in murine bone marrow-derived stromal cell lines, normal human bone-derived cells, and nontransformed osteoblast cell lines from mice and rats. In all these cell types IL-6 production was stimulated as much as 10,000-fold in response to the combination of recombinant interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF alpha). Addition of 17 beta-estradiol in the cultures exerted a dose-dependent inhibition of IL-1-, TNF-, and IL-1 + TNF-induced production of bioassayable IL-6. Testosterone and progesterone (but not 17 alpha-estradiol) also inhibited IL-6, but their effective concentrations were two orders of magnitude higher than 17 beta-estradiol. 17 beta-estradiol also decreased the levels of the IL-6 mRNA. In addition, estradiol inhibited both TNF-induced IL-6 production and osteoclast development in primary bone cell cultures derived from neonatal murine calvaria. The TNF-stimulated osteoclast development was also suppressed by a neutralizing monoclonal anti-IL-6 antibody. This in vitro evidence suggests, for the first time, a mechanistic paradigm by which estrogens might exert at least part of their antiresorptive influence on the skeleton.

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