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Published ahead of print on February 19, 2004, doi:10.1165/rcmb.2003-0299OC

Am. J. Respir. Cell Mol. Biol., Volume 31, Number 1, July 2004, 78-85

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Submitted on August 13, 2003
Revised on February 19, 2004

CHARACTERIZATION OF THE EFFECT OF INTERLEUKIN-10 (IL-10) ON SILICA-INDUCED LUNG FIBROSIS IN MICE

Virginie Barbarin1, Mohammed Arras1, Pierre Misson1, Monique Delos2, Bridget McGarry3, Sem H Phan3, Dominique Lison1, and Francois Huaux4*

1 Industrial Toxicology and Occupational Medicine Unit, Universite Catholique de Louvain, Faculte de Medecine, Brussels, Belgium, 2 University Hospital of Mont Godinne, Laboratory of Pathology, Universite Catholique de Louvain, Faculte de Medecine, Yvoir, Belgium, 3 Department of Pathology, University of Michigan, Ann Arbor, Michigan, USA, 4 Industrial Toxicology and Occupational Medicine Unit, Universite Catholique de Louvain, Faculte de Medecine, Brussels, Belgium; University Hospital of Mont Godinne, Laboratory of Pathology, Universite Catholique de Louvain, Faculte de Medecine, Yvoir, Belgium

* To whom correspondence should be addressed. E-mail: huaux{at}toxi.ucl.ac.be.

We previously described a reduction of silica-induced lung fibrosis in IL-10 deficient mice (IL-10-/-) (Huaux and colleagues ; Am. J. Respir. Cell Mol. Biol. 1998; 18:51-59). In the present study, we further dissect the exact functions of IL-10 in experimental silicosis. The reduced lung fibrotic response to silica in IL-10-/- mice was accompanied by a marked recruitment of TH1 CD4+ lymphocytes. However treatment with anti-CD4 antibodies reduced silica-induced lung fibrosis in both IL-10-/- and IL-10+/+ mice, suggesting that this T cell population actually contributes to the extension of the fibrotic lesions in a manner that is independent of IL-10. In IL-10-/- mice, silica-induced lung production of the pro-fibrotic mediator TGF-{beta}1 and the anti-fibrotic eicosanoid PGE2 were reduced and increased, respectively, relative to that in IL-10+/+ mice. In addition, in vitro experiments indicated that recombinant IL-10 upregulated TGF-{beta}1 expression in alveolar macrophages while in contrast, it downregulated PGE2 production and COX-2 expression in both lung fibroblasts and macrophages. Thus the net pro-fibrotic activity of IL-10 in vivo appears to be mediated by its ability to stimulate the expression of the pro-fibrotic cytokine, TGF-{beta}1 while suppressing the expression of COX2 and thus production of the anti-fibrotic eicosanoid, PGE2. These effects appear to be independent of the enhanced lung CD4+ T-lymphocytosis observed in IL-10 deficient mice.




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