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-Induced IL-6 Expression 1
Departments of
*
Medicine and
Pathology, Division of Pulmonary and Critical Care Medicine, and
Division of Cell Biology, University of Alabama, Birmingham AL 35294;
Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, TN 37205;
¶
Department of Internal Medicine, University Hospital of Geneva, Geneva, Switzerland; and
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Cardiovascular Research Institute, University of California, San Francisco, CA 94143
Although the fibroproliferative response to lung injury occurs with a high frequency in patients with clinical acute lung injury, the mechanisms that initiate this response are largely unknown. This study was undertaken first to identify fibroblast mitogenic factors in pulmonary edema fluid, and second to examine the human lung fibroblast’s gene expression profile in response to pulmonary edema fluid. The edema fluid obtained from patients with early lung injury has an eightfold higher concentration of IL-1
and a twofold greater IL-1-dependent mitogenic effect than does fluid obtained from control patients with hydrostatic pulmonary edema. Furthermore, fibroblasts responded to acute lung injury patient-derived edema fluid through production of soluble mediators that possess an autocrine mitogenic effect. Gene array analysis reveals that acute lung injury edema fluid induces several inflammation-modulating and proliferation-related genes in fibroblasts, whose inductions are similarly dependent on bioactive IL-1. Most notably, the 20-fold induction of IL-6 mRNA and protein was completely blocked by IL-1 receptor antagonist. The combined addition of IL-1 and IL-6 was mitogenic, and the proliferative response to conditioned medium from IL-1-exposed cells was blocked by antagonistically acting Abs to IL-6 or to gp130. These novel findings indicate that soluble IL-1 bioactivity and autocrine IL-1-dependent IL-6 up-regulation are critical initiators of fibroblast activation and proliferation and that they likely play a role in the fibroproliferative response seen in human acute lung injury.
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