論文 - 詳細
| RRC ID | 6042 |
|---|---|
| 著者 | Giordano G, van den Brûle S, Lo Re S, Triqueneaux P, Uwambayinema F, Yakoub Y, Couillin I, Ryffel B, Michiels T, Renauld JC, Lison D, Huaux F. |
| タイトル | Type I interferon signaling contributes to chronic inflammation in a murine model of silicosis. |
| ジャーナル | Toxicol Sci |
| 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. |
| 巻・号 | 116(2) |
| ページ | 682-92 |
| 公開日 | 2010-8-1 |
| DOI | 10.1093/toxsci/kfq158 |
| PII | kfq158 |
| PMID | 20513754 |
| MeSH | Animals Chronic Disease Dendritic Cells / physiology Disease Models, Animal Inflammation / etiology* Interferon Type I / physiology* Macrophages / physiology Mice Mice, Inbred C57BL Signal Transduction* Silicosis / immunology* |
| IF | 3.703 |
| 引用数 | 22 |
| WOS 分野 | TOXICOLOGY |
| オルトメトリクス指標 |
オルトメトリクス指標項目
|
| 各媒体での言及数の合計 | 0 |
| リソース情報 | |
| 実験動物マウス | RBRC01420 |