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Regulation of CCAAT/Enhancer-Binding Protein-β Is Altered in Primary Lung Fibroblasts Obtained From Patients With Idiopathic Pulmonary Fibrosis*

Roberto A. Cruz-Gervis, MD; Arlene A. Stecenko, MD; Timothy S. Blackwell, MD, FCCP; Linda Sealy, PhD; James E. Loyd, MD; Gayle King; Kenneth L. Brigham, MD
Author and Funding Information

*From the Center for Lung Research, Vanderbilt University Medical Center, Nashville, TN.

Correspondence to: Roberto A. Cruz-Gervis, MD, Division of Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center, MCN T-1217, Nashville TN 37232-2650



Chest. 2001;120(1_suppl):S9. doi:10.1378/chest.120.1_suppl.S9
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Since BAL fluid interleukin (IL)-6 levels are elevated in multiple chronic inflammatory and fibrotic lung diseases, and since stimulated lung fibroblasts produced large amounts of IL-6 in vitro, these cells may represent a major source of this cytokine. Nuclear factor (NF)-κB and CCAAT/enhancer-binding protein-β (C/EBP-β) are necessary for maximal transcription of IL-6, and the latter has also been shown to induce gene expression of profibrotic factors, namely insulin-like growth factor-1 and collagen I. For those reasons, we asked whether primary lung fibroblasts obtained from lung of patients with idiopathic pulmonary fibrosis (HF-IPF) could have an altered regulation of these transcription factors compared with fibroblasts obtained from normal human lungs (HF-NL).

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