Type I Interferon Signaling Contributes to Chronic Inflammation in a Murine Model of Silicosis

Giordano, Giulia;Van Den Brûle, Sybille;Lo Re, Sandra;Triqueneaux, Perrine;Huaux, François;et.al.
(2010) Toxicological Sciences — Vol. 116, n° 2, p. 682-692 (2010)

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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.
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Giordano, G., Van Den Brûle, S., Lo Re, S., Triqueneaux, P., Uwambayinema, F., Yakoub, Y., Couillin, I., Ryffel, B., Michiels, T., Renauld, J.-C., Lison, D., & Huaux, F. (2010). Type I Interferon Signaling Contributes to Chronic Inflammation in a Murine Model of Silicosis. Toxicological Sciences, 116(2), 682-692. https://doi.org/10.1093/toxsci/kfq158 (Original work published 2010)