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1 Industrial Toxicology and Occupational Medicine Unit, Universite catholique de Louvain, Faculty of Medicine, Brussels, Belgium
2 Department of Pathology, McMaster University, Hamilton, Canada
3 Laboratory of Pathology, Universite catholique de Louvain, University Hospital of Mont-Godinne, Yvoir, Belgium
* To whom correspondence should be addressed. E-mail: huaux{at}toxi.ucl.ac.be.
Chronic inflammation and pro-inflammatory 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 d-1) or the fibrotic (administered at d+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
BALF IgG1 but not IgG2a levels, indicating the induction of a TH2-like immune response. In addition, the production of the pro-fibrotic TH2 cytokines IL-4 and IL-13 was also
significantly increased upon IL-10 overexpression. No difference in TGF-
or PGE2 production was noted after AdIL-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 pro-fibrotic cytokines IL-4 and IL-13.
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