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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Tilg, H Articles by Mier, J. Search for Related Content PubMed PubMed Citation Articles by Tilg, H Articles by Mier, J. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Interleukin-6 (IL-6) as an anti-inflammatory cytokine: induction of circulating IL-1 receptor antagonist and soluble tumor necrosis factor receptor p55 H Tilg, E Trehu, MB Atkins, CA Dinarello and JW Mier Department of Medicine, New England Medical Center, Boston, MA 02111. The aim of this study was to investigate whether interleukin (IL)-6 induces the production of IL-1 and tumor necrosis factor (TNF) antagonists. Serial plasma samples were obtained from cancer patients participating in phase I and II trials of recombinant IL-6 administered as a 120-hour continuous intravenous (IV) infusion. Plasma IL-1 receptor antagonist (IL-1Ra) and soluble TNF receptor p55 (TNFsRp55) levels were measured by specific radioimmunoassays (RIAs). IL-1Ra levels increased rapidly, reaching peak values (9.6 +/- 1.7 ng/mL) within 2 to 4 hours of beginning treatment. Thereafter, levels promptly declined, reaching near baseline within 24 hours despite continuation of IL-6. TNFsRp55 plasma levels increased within 4 to 8 hours after initiating treatment and increased progressively throughout the duration of therapy. IL-1 beta and TNF-alpha plasma levels were below the detection limit in all samples tested. Peripheral blood mononuclear cells (PBMC) exposed to IL-6 produced only small amounts (1.56 +/- 0.3 ng/mL) of IL-1Ra, even in the presence of exogenous soluble IL-6 receptor (gp80). TNFsRp55 levels measured in the supernatants of IL-6- stimulated PBMC were below the detection limit of the assay. Macrophages generated by culturing monocytes in granulocyte-macrophage colony-stimulating factor (GM-CSF) were much more responsive to IL-6 than freshly isolated unfractionated or adherent PBMC and synthesized almost as much IL-1Ra when stimulated with IL-6 as with endotoxin. These results suggest that the antinflammatory properties of IL-6 may be due; in part, to the induction of IL-1Ra synthesis and the release of soluble TNF receptors. Our findings also suggest that tissue macrophages may be an important source of IL-6-induced IL-1Ra. Volume 83, Issue 1, pp. 113-118, 01/01/1994 Copyright © 1994 by The American Society of Hematology CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Holm, Z. Mackiewicz, A. K. Holm, Y. T. Konttinen, V.-P Kouri, A. Indahl, and J. Salo Pro-inflammatory, Pleiotropic, and Anti-inflammatory TNF-{alpha}, IL-6, and IL-10 in Experimental Porcine Intervertebral Disk Degeneration Vet. Pathol., November 1, 2009; 46(6): 1292 - 1300. [Abstract] [Full Text] [PDF] M. T. Haren, T. K. Malmstrom, D. K. Miller, P. Patrick, H. M. Perry III, M. M. Herning, W. A. Banks, and J. E. Morley Higher C-Reactive Protein and Soluble Tumor Necrosis Factor Receptor Levels Are Associated With Poor Physical Function and Disability: A Cross-Sectional Analysis of a Cohort of Late Middle-Aged African Americans J Gerontol A Biol Sci Med Sci, October 7, 2009; (2009) glp148v1. [Abstract] [Full Text] [PDF] R. A. Johnston, T. A. Theman, F. L. 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