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IL-6 Negatively Regulates IL-11 Production in Vitro and in Vivo

Department of Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-8020

Address all correspondence and requests for reprints to: Karl Insogna, M.D., Section of Endocrinology, Department of Medicine, Yale University School of Medicine, 333 Cedar Street, FMP 106, P.O. Box 208020, New Haven, Connecticut 06520-8020. E-mail: karl.insogna{at}yale.edu

IL-6 and IL-11 are two cytokines that increase osteoclast formation and augment bone resorption. PTH stimulates the production of both cytokines by human osteoblast-like cells. Circulating levels of IL-6 are elevated in patients with states of PTH excess and correlate strongly to markers of bone resorption. In contrast, serum levels of IL-11 were significantly reduced in patients with primary hyperparathyroidism compared with values in euparathyroid controls. Further, after successful parathyroid adenomectomy, circulating levels of IL-6 fell, whereas IL-11 levels increased. Five-day infusions of human PTH-(1–84) in rodents resulted in a significant decline in mean circulating levels of IL-11, whereas IL-6 levels significantly increased. Pretreatment of cells and mice with neutralizing serum to IL-6 enhanced PTH-induced IL-11 production compared with the effect of pretreatment with nonimmune sera. These data indicate that IL-6 negatively regulates IL-11 production in vivo and in vitro. Analysis of steady state mRNA levels in SaOS-2 cells indicated that this effect is posttranscriptional. As both IL-6 and IL-11 stimulate osteoclast formation, down-regulation of IL-11 by IL-6 may help modulate the resorptive response to PTH.

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				U. S. Masiukiewicz, M. Mitnick, B. I. Gulanski, and K. L. Insogna Evidence that the IL-6/IL-6 Soluble Receptor Cytokine System Plays a Role in the Increased Skeletal Sensitivity to PTH in Estrogen-Deficient Women J. Clin. Endocrinol. Metab., June 1, 2002; 87(6): 2892 - 2898. [Abstract] [Full Text] [PDF]