Human Fibroblasts Produce Granulocyte-CSF, Macrophage-CSF, and Granulocyte-Macrophage-CSF Following Stimulation by Interleukin-1 and Poly(rI).Poly(rC)
Electrophoretically pure human interleukin-1 (IL-1) beta was found to stimulate human fibroblasts in a monolayer culture to elaborate colony-stimulating activity (CSA). Supernatant fluids from cultures induced with increasing concentrations of IL-1 were found to stimulate colony formation of myeloid...
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Published in: | Blood Vol. 72; no. 3; pp. 860 - 866 |
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Main Authors: | , , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Washington, DC
Elsevier Inc
01-09-1988
The Americain Society of Hematology |
Subjects: | |
Online Access: | Get full text |
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Summary: | Electrophoretically pure human interleukin-1 (IL-1) beta was found to stimulate human fibroblasts in a monolayer culture to elaborate colony-stimulating activity (CSA). Supernatant fluids from cultures induced with increasing concentrations of IL-1 were found to stimulate colony formation of myeloid (CFU-GM), erythroid (BFU-E), and multipotent (CFU-GEMM) progenitor cells in a dose-depen-dent fashion. The effect on mixed colony formation, however, was less than on CFU-GM and BFU-E growth. Similar to IL-1, the synthetical double-stranded RNA poly(rl).poly(rC) also stimulated release of CSA by fibroblasts. The kinetics of IL-1- and poly(rl).poly(rC)-induced CSA release were found to be different, in that poly(rl).poly(rC)-induced CSA production occurred more slowly. Anti-IL-1 antiserum was able to completely neutralize the IL-1 -induced CSA release, but had no effect on poly(rl).poly(rC)-induced CSF production, suggesting that the latter effect was mediated by other mechanisms than IL-1 in supernatant. By the use of specific immunologic assays, G-CSF, M-CSF, and GM-CSF could be identified in media conditioned by fibroblasts treated with IL-1 or poly(rl).poly(rC). Poly(rl).poly(rC) appeared to be a better inducer for M-CSF than IL-1.1988 by Grune & Stratton, Inc. 0006-4971/88/7203-0001$3.00/0. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0006-4971 1528-0020 |
DOI: | 10.1182/blood.V72.3.860.860 |