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Increase in laminin expression in allergic airway remodelling and decrease by dexamethasone

Depts of ¹ Medicine and ² Pathology, University of Washington, Seattle, WA, USA. ³ Dept of Pathology, Chung Shan Medical and Dental University, Taichung, Taiwan

CORRESPONDENCE: W.R. Henderson Jr, Dept of Medicine, Box 356523, University of Washington, 1959 NE Pacific Street, Seattle, WA 98195-6523, USA. Fax: 1 2066859318. E-mail: joangb@u.washington.edu

Keywords: Allergy, eosinophils, extracellular matrix, fibrosis, inflammation

Received: February 5, 2003
Accepted February 7, 2004

This study was supported by National Institutes of Health (Bethesda, MD, USA) grants AI42989 and HL73722.

Lung expression of the extracellular matrix protein, laminin, and its receptor, laminin-1 receptor, were examined in a mouse model of asthma with airway remodelling.

Ovalbumin (OVA) was administered to BALB/c mice, intraperitoneally on days 0 and 14, and intranasally periodically between days 14 and 75.

The mice developed airway eosinophil and mononuclear inflammatory cell infiltration and fibrosis. On day 76, a marked increase in total laminin was seen in the airways of OVA-treated mice compared to controls by Western blot analysis. The increased laminin expression was detected immunocytochemically in the thickened subepithelial basement membrane and around airways and blood vessels. The OVA-treated mice showed increased expression of the 1, ß1, and 1 chains of the laminin-1 isoform in monocytes, macrophages and eosinophils infiltrating the airways. Laminin-1 receptor expression was increased in inflammatory and endothelial cells in the lungs of OVA-treated mice compared to controls. Treatment of OVA-sensitised/challenged mice with dexamethasone reduced airway expression of laminin and laminin-1 receptor in OVA-treated mice but not airway hyperresponsiveness to methacholine.

Laminin deposition may be an important component of the airway remodelling observed in chronic allergic lung inflammation and is a process modulated by corticosteroids.

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