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Originally published online as doi:10.2353/ajpath.2009.080689 on April 9, 2009

Published online before print April 9, 2009
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(American Journal of Pathology. 2009;174:1683-1691.)
© 2009 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2009.080689

Essential Role of Osteopontin in Smoking-Related Interstitial Lung Diseases

Antje Prasse*, Mirjam Stahl*, Guido Schulz{dagger}, Gian Kayser{ddagger}, Lingqiao Wang§, Kjetil Ask§, Jasmin Yalcintepe*, Andreas Kirschbaum, Elena Bargagli||, Gernot Zissel*, Martin Kolb§, Joachim Müller-Quernheim*, Johannes M. Weiss{dagger} and Andreas C. Renkl{dagger}

From the Department of Pneumology,* University Medical Center Freiburg, Freiburg, Germany; the Department of Dermatology,{dagger} University Hospital Ulm, Ulm, Germany; the Departments of Pathology,{ddagger} and Thoracic Surgery, University Hospital Freiburg, Freidburg, Germany; the Departments of Medicine, Pathology and Molecular Medicine,§ McMaster University, Hamilton, Canada; and the Dipartimento di Medicina Clinica e Scienze,|| Immunologiche, Sezione di Malattie dell Apparato Respiratorio, University of Siena, Siena, Italy

Smoking-related interstitial lung diseases are characterized by the accumulation of macrophages and Langerhans cells, and fibrotic remodeling, which are linked to osteopontin (OPN) expression. Therefore, OPN levels were investigated in bronchoalveolar lavage (BAL) cells in 11 patients with pulmonary Langerhans cell histiocytosis (PLCH), 15 patients with desquamative interstitial pneumonitis (DIP), 10 patients with idiopathic pulmonary fibrosis, 5 patients with sarcoidosis, 13 otherwise healthy smokers, and 19 non-smoking controls. Furthermore, OPN overexpression was examined in rat lungs using adenoviral gene transfer. We found that BAL cells from patients with either PLCH or DIP spontaneously produced abundant amounts of OPN. BAL cells from healthy smokers produced 15-fold less OPN, and those cells from non-smoking healthy volunteers produced no OPN. BAL cells from patients with either idiopathic pulmonary fibrosis or sarcoidosis produced significantly less OPN, as compared with patients with PLCH. These data were confirmed by immunochemistry. Nicotine stimulation increased production of both OPN and granulocyte-macrophage colony stimulating factor by alveolar macrophages from smokers. Nicotinic acetylcholine receptor expression resembled the pattern of spontaneous OPN production and was dramatically increased in both PLCH and DIP. OPN overexpression in rat lungs induced lesions similar to PLCH with marked alveolar and interstitial accumulation of Langerhans cells. Our findings suggest a pathogenetic role of increased OPN production in both PLCH and DIP by promoting the accumulation of macrophages and Langerhans cells.


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