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Toxicol Sci. 2010 Aug;116(2):682-92. doi: 10.1093/toxsci/kfq158. Epub 2010 May 31.

Type I interferon signaling contributes to chronic inflammation in a murine model of silicosis.

Author information

1
Louvain Centre for Toxicology and Applied Pharmacology, Université catholique de Louvain, 1200 Brussels, Belgium.

Abstract

Lung disorders induced by inhaled inorganic particles such as crystalline silica are characterized by chronic inflammation and pulmonary fibrosis. Here, we demonstrate the importance of type I interferon (IFN) in the development of crystalline silica-induced lung inflammation in mice, revealing that viruses and inorganic particles share similar signaling pathways. We found that instillation of silica is followed by the upregulation of IFN-beta and IRF-7 and that granulocytes (GR1(+)) and macrophages/dendritic cells (CD11c(+)) are major producers of type I IFN in response to silica. Two months after silica administration, both IFNAR- and IRF-7-deficient mice produced significantly less pulmonary inflammation and chemokines (KC and CCL2) than competent mice but developed similar lung fibrosis. Our data indicate that type I IFN contributes to the chronic lung inflammation that accompanies silica exposure in mice. Type I IFN is, however, dispensable in the development of silica-induced acute lung inflammation and pulmonary fibrosis.

PMID:
20513754
DOI:
10.1093/toxsci/kfq158
[Indexed for MEDLINE]

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