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Keratinocyte growth factor improves alterations of lung permeability and bronchial epithelium in allergic rats

¹ INSERM U774, Institut Pasteur, Lille- and Université de Lille II, ² Laboratory of Infectious Pathology Research, and ⁴ Laboratory of Biophysics, CHRU de Lille, Lille, and ³ Laboratory of Pathology, U728 Inserm, Université Paris 7, Hopital Saint Louis, Paris, France, ⁵ I. Tillie-Leblond and P. Gosset contributed equally to this manuscript.

CORRESPONDENCE: P. Gosset, INSERM U774, Institut Pasteur, 1 rue Calmette, BP245, 59019-Lille Cedex, France. Fax: 33 320877345. E-mail: philippe.gosset{at}pasteur-lille.fr

Keywords: Asthma, growth factor, inflammation, lung permeability, rat

Received: January 25, 2006
Accepted March 22, 2007

Chronic allergic asthma is associated with marked inflammatory reaction, microvascular leakage and epithelium injury. As previously shown in a rat model of chronic asthma, these alterations increase lung permeability and distal airway fluid clearance. Keratinocyte growth factor (KGF) has been shown to induce epithelial cell proliferation and to protect from acute lung injuries. Therefore, the current authors evaluated the potential role of KGF treatment on lung permeability and airway inflammation in rats with chronic asthma.

KGF (1 mg·kg^–1) was administered intravenously before the last ovalbumin (OVA) challenge in sensitised rats. Permeability was assessed by the leak of radiolabelled albumin from the alveolar and systemic compartments. Histopathological analysis was also performed.

Treatment with KGF decreased the leak of both markers and decreased the level of extravascular lung water in sensitised rats challenged with OVA. KGF treatment also reduced the inflammatory cell number in bronchoalveolar lavage fluid but not in bronchial mucosa. KGF markedly limited the allergen-induced alterations in epithelium integrity and the expression of the intercellular junction proteins ß-catenin and zonula occludens protein-1.

In conclusion, keratinocyte growth factor administration markedly limits lung permeability and airway inflammation, an effect associated with a decrease in epithelium alterations during chronic allergic asthma. These data open new prospects in the therapeutic strategy of asthma.

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