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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted 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 Chen, B. D. Search for Related Content PubMed PubMed Citation Articles by Chen, B. D. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  In vivo administration of recombinant human interleukin-1 and macrophage colony-stimulating factor (M-CSF) induce a rapid loss of M- CSF receptors in mouse bone marrow cells and peritoneal macrophages: effect of administration route BD Chen Department of Internal Medicine, Wayne State University School of Medicine, Detroit, MI 48201. Earlier studies suggested the existence of a blood-bone marrow barrier that significantly inhibits the transfer of plasma macrophage colony- stimulating factor (M-CSF) to responsive hematopoietic cells in vivo as indicated by its failure to induce a receptor downregulation in bone marrow cells. In this study, the effect of recombinant human interleukin-1 (rhuIL-1) was investigated. In vivo administration of rhuIL-1, either intraperitoneally (IP) or intravenously (IV), induced a rapid transient loss of M-CSF receptor binding activity in bone marrow cells, with a nadir occurring between 2 to 4 hours while loss of M-CSF receptors by cells in the peritoneal cavity occurred only in animals receiving rhuIL-1 via IP administration. The loss of M-CSF receptor activity after rhuIL-1 treatment was correlated with an elevated level of circulating M-CSF. However, the loss of M-CSF receptors in marrow cells was prevented by dexamethasone (Dex) treatment before rhuIL-1 administration. The fact that Dex treatment also reduced the level of circulating M-CSF after rhuIL-1 administration suggests that the inhibitory effects of IL-1 are mediated through locally produced M-CSF. Administration of rhuM-CSF at higher doses, either IV or IP, also induced a loss of M-CSF receptor of lesser degree in the marrow cells. However, the loss of M-CSF receptors by the peritoneal cells was induced only in mice receiving rhuM-CSF through IP administration. Taken together, these results indicate the existence of a unidirectional barrier that prevents the transfer of blood M-CSF and IL- 1 to peritoneal cavity but not vice versa. Volume 77, Issue 9, pp. 1923-1928, 05/01/1991 Copyright © 1991 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: I. O. Gordon and R. S. Freedman Defective Antitumor Function of Monocyte-Derived Macrophages from Epithelial Ovarian Cancer Patients Clin. Cancer Res., March 1, 2006; 12(5): 1515 - 1524. [Abstract] [Full Text] [PDF] M. Cecchini, M. Dominguez, S Mocci, A Wetterwald, R Felix, H Fleisch, O Chisholm, W Hofstetter, J. Pollard, and E. Stanley Role of colony stimulating factor-1 in the establishment and regulation of tissue macrophages during postnatal development of the mouse Development, January 6, 1994; 120(6): 1357 - 1372. [Abstract] [PDF]

	Copyright © 1991 by American Society of Hematology         Online ISSN: 1528-0020