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Localization of Insulin-like Growth Factor-I in Lung Tissues of Patients with Fibroproliferative Acute Respiratory Distress Syndrome

Department of Medicine, Immunology Research Group, and Departments of Surgery, Pathology, Biochemistry and Molecular Biology, and Critical Care Medicine, University of Calgary, Health Sciences Center, Calgary, Alberta, Canada

Correspondence and requests for reprints should be addressed to Brent W. Winston, M.D., Departments of Medicine, Critical Care Medicine, and Biochemistry and Molecular Biology, University of Calgary, Health Sciences Center, Room 1843, 3330 Hospital Drive N.W., Calgary, AB, T2N 4N1 Canada. E-mail: bwinston{at}ucalgary.ca

Insulin-like growth factor-I (IGF-I) is elevated in human fibrotic lung diseases and in animal models of pulmonary fibrosis, implicating IGF-I in the pathogenesis of fibrotic lung disease. We questioned whether IGF-I protein levels were enhanced in fibroproliferative acute respiratory distress syndrome (FP-ARDS). Serial lung tissue sections from a biopsy database were immunohistochemically stained for IGF-I, IGF-I receptor, CD68, -smooth muscle actin, collagens I and III, and proliferating cell nuclear antigen. Our results show enhanced staining of IGF-I and IGF-I receptor, collagens I and III, smooth muscle actin, CD68, and proliferating cell nuclear antigen in FP-ARDS compared with control lung sections. In FP-ARDS specimens, prominent staining of IGF-I and IGF-I receptor was seen in alveolar and interstitial macrophages as well as in a variety of mesenchymal cells. There was a correlation between IGF-I staining and CD68-positive cells, suggesting macrophages as a potential source of the IGF-I protein present in lungs. IGF-I also correlated with enhanced collagen I, collagen III, and proliferating cell nuclear antigen immunoreactivity, suggesting that IGF-I may play a role in the extracellular matrix protein deposition and cellular proliferation seen in the lungs of individuals with FP-ARDS. Our results indicate that IGF-I is increased in FP-ARDS and may be an important mediator in the progression of acute lung injury to FP-ARDS.

Key Words: acute respiratory distress syndrome • insulin-like growth factor-I • macrophage • pulmonary fibrosis

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