Induction of fibroblast proliferation by interleukin-1 derived from human monocytic leukemia cells

Authors

  • Arnold E. Postlethwaite MD,

    Corresponding author
    1. From the Laboratory of Cellular Immunology and the Medical Service, Veterans Administration Medical Center, the Departments of Medicine and Biochemistry, University of Tennessee Center for the Health Sciences, Memphis and the Department of Cell Biology, M. D. Anderson Hospital, Houston, Texas.
    • Research Service (151), VA Medical Center, 1030 Jefferson Avenue, Memphis, TN 38104
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  • Lawrence B. Lachman PhD,

    1. From the Laboratory of Cellular Immunology and the Medical Service, Veterans Administration Medical Center, the Departments of Medicine and Biochemistry, University of Tennessee Center for the Health Sciences, Memphis and the Department of Cell Biology, M. D. Anderson Hospital, Houston, Texas.
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  • Andrew H. Kang MD

    1. From the Laboratory of Cellular Immunology and the Medical Service, Veterans Administration Medical Center, the Departments of Medicine and Biochemistry, University of Tennessee Center for the Health Sciences, Memphis and the Department of Cell Biology, M. D. Anderson Hospital, Houston, Texas.
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Abstract

Human interleukin-1 (IL-1), free of contaminating lymphokines, was isolated from cultures of purified monoblasts from a patient with acute monocytic leukemia. Partially purified IL-1 (diafiltration, ultrafiltration, and isoelectric focusing) stimulated proliferation of subconfluent human fibroblasts in vitro. Further purification of IL-1 by high-resolution gel filtration- and anion exchange-high performance liquid chromatography revealed that fibroblast proliferation activity could not be separated from IL-1 activity (thymocyte proliferation), suggesting that both activities are the properties of a single molecule. Fibroblasts and thymocytes exhibited a similar sensitivity to the proliferative effects of IL-1. These findings suggest that macrophages participating in inflammatory reactions in vivo might release IL-1, which could function to expand fibroblast populations at sites of inflammatory reactions, by acting as a fibroblast growth factor.

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