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Articles in PresS, published online ahead of print July 19, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00107.2002
Submitted on April 10, 2002
Accepted on June 11, 2002
1 Lung Cellular & Molecular Biology Laboratory-Institute of Pulmonology, Hadassah University Hospital and The Hebrew University-Hadassah Medical School, Jerusalem, Israel
2 Bone Marrow Transplantion Department, Hadassah University Hospital and The Hebrew University-Hadassah Medical School, Jerusalem, Israel
3 Mallory Institute of Pathology, Department of Pathology, Boston University School of Medicine and Boston VA Medical Center, Boston, MA, USA
4 Department of Pulmonary, Boston University School of Medicine and Boston VA Medical Center, Boston, MA, USA
5 Lung Cellular & Molecular Biology Laboratory-Institute of Pulmonology, Hadassah University Hospital and The Hebrew University-Hadassah Medical School, Jerusalem, Israel; Mallory Institute of Pathology, Department of Pathology, Boston University School of Medicine and Boston VA Medical Center, Boston, MA, USA; Department of Pulmonary, Boston University School of Medicine and Boston VA Medical Center, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: rgoldstein{at}lung.bumc.bu.edu.
The role of IL-4 in the development of lung fibrosis is as yet unclear. Bleomycin (Bleo) or saline (Sal) was injected intratracheally into 3 groups of C57Bl/6J mice: transgenic animals that overexpressed IL-4 (IL-4 TG) (n = 14), mice with a targeted knockout mutation of the IL-4 gene (IL-4 KO) (n = 11), and wild-type (WILD) (n = 13) mice. At 14 days, lung fibrosis was evaluated by hydroxyproline measurement and by quantitative image analysis of fibrosis fraction and alveolar wall area fraction. BAL cell counts in all Bleo-treated groups demonstrated an increased percentage of lymphocytes with a corresponding decrease in the percentage of macrophages. Comparing Bleo- to Sal-treated controls within each group of mice showed increases in all lung fibrosis parameters in IL-4 KO and WILD, but not in any of the parameters in IL-4 TG mice. The severity of Bleo-induced fibrotic response was decreased in overexpressed IL-4 TG compared with IL-4 KO mice. These data negate a critical pro-fibrotic role for IL-4 in Bleo-induced lung fibrosis.
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