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Published ahead of print on January 27, 2005, doi:10.1165/rcmb.2004-0205OC

Am. J. Respir. Cell Mol. Biol., Volume 32, Number 5, May 2005, 470-477

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Submitted on June 24, 2004
Revised on January 24, 2005

KGF expression by fibroblasts in pulmonary fibrosis: poor response to interleukin-1 beta

Sylvain Marchand-Adam1, Laurent Plantier1, Dominique Bernuau2, Agnes Legrand2, Murielle Cohen3, Joelle Marchal1, Paul Soler1, Guy Leseche4, Herve Mal5, Michel Aubier6, Monique Dehoux3, and Bruno Crestani6*

1 Unit 700, INSERM, Paris, France, 2 Unit 327, INSERM, Paris, France, 3 Unit 700, INSERM, Paris, France; Service de biochimie 1, Hopital Bichat, Assistance Publique-Hopitaux de Paris, Paris, France, 4 Service de Chirurgie thoracique et cardio-vasculaire, Hopital Beaujon, Assistance Publique-Hopitaux de Paris, Clichy, France, 5 Unit 700, INSERM, Paris, France; Service de Pneumologie, Hopital Beaujon, Assistance Publique-Hopitaux de Paris, Clichy, France, 6 Unit 700, INSERM, Paris, France; Service de Pneumologie, Hopital Bichat, Assistance Publique-Hopitaux de Paris, Paris, France

* To whom correspondence should be addressed. E-mail: bruno.crestani{at}bch.ap-hop-paris.fr.

Keratinocyte growth factor (KGF) is secreted by fibroblasts and protects from pulmonary fibrosis in animal models. IL-1{beta} is the most potent inducer of KGF in fibroblasts, acting through the c-Jun pathway. We evaluated in vitro KGF production by human lung fibroblasts from patients with idiopathic pulmonary fibrosis (IPF, n=10) and from controls (n=7) at baseline and after IL-1{beta} stimulation. Basal KGF secretion by IPF fibroblasts was similar to controls. In controls fibroblasts, IL-1{beta} increased c-Jun expression, c-Jun activation, and KGF secretion. SP600125, a specific c-Jun N terminal kinase (JNK) inhibitor, inhibited the effect of IL-1{beta}. By contrast, in IPF fibroblasts, IL-1{beta} did not increase c-Jun expression and c-Jun activation, and weakly increased KGF secretion, whereas SP600125 had no effect. IL-1{beta} similarly increased JunB expression in IPF and controls fibroblasts. Total JNK content was not different in either unstimulated or IL-1{beta} stimulated IPF and control fibroblasts. IL-1{beta} increased phosphorylated JNK in control and IPF fibroblasts, but this increase was weaker and heterogeneous in IPF. Altogether, our results demonstrate a dysregulation of KGF secretion by IPF fibroblasts. The weak response to IL-1{beta} is associated with a defect of c-Jun expression and activation and a defect of JNK activation.




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