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Am J Physiol Lung Cell Mol Physiol 288: L841-L848, 2005. First published December 17, 2004; doi:10.1152/ajplung.00329.2004
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Pulmonary overexpression of IL-10 augments lung fibrosis and Th2 responses induced by silica particles

Virginie Barbarin,1 Zhou Xing,2 Monique Delos,3 Dominique Lison,1 and Francois Huaux1

1Industrial Toxicology and Occupational Medicine Unit, Faculty of Medicine; 3Laboratory of Pathology, University Hospital of Mont Godinne, Yvoir, Université catholique de Louvain, Brussels, Belgium; and 2Department of Pathology, McMaster University, Hamilton, Ontario, Canada

Submitted 1 September 2004 ; accepted in final form 10 December 2004

Chronic inflammation and proinflammatory cytokines as well as T helper type 2 (Th2) cytokines have been involved in the pathogenesis of pulmonary injury and lung fibrosis. The actual role of IL-10 in lung fibrosis is still unclear because this cytokine has been identified as Th2 but possesses strong anti-inflammatory properties. To better dissect the potential role of IL-10 in silica-induced lung fibrosis, IL-10 was overexpressed in the lung of mice by adenoviral gene transfer during the inflammatory (administered at day –1) or the fibrotic (administered at day +30) stages of the disease. Pulmonary overexpression of IL-10 during both silica-induced lung inflammation and fibrosis exacerbated the fibrotic lesions as estimated by the measurement of hydroxyproline and other biochemical and histological markers. Increased expression of IL-10 significantly enhanced the number of lung lymphocytes and bronchoalveolar lavage fluid IgG1 but not IgG2a levels, indicating the induction of a Th2-like immune response. In addition, the production of the profibrotic Th2 cytokines IL-4 and IL-13 was also significantly increased upon IL-10 overexpression. No difference in transforming growth factor-{beta} or PGE2 production was noted after adenoviral IL-10 treatment of silica-treated mice. Together, these data indicate that the increased expression of IL-10 significantly contributed to silica-induced lung fibrosis by exacerbating the Th2 response and the production of the profibrotic cytokines IL-4 and IL-13.

inflammation; T helper 2 cytokines; interleukin-10


Address for reprint requests and other correspondence: F. Huaux, Unit of Industrial Toxicology and Occupational Medicine, Université Catholique de Louvain, 30.54, Clos Chapelle-aux-Champs, 1200 Brussels, Belgium (E-mail: huaux{at}toxi.ucl.ac.be)




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