Abstract
THE deposition of silica particles in the lung of man or experimental animals leads to silicosis, a disease of progressive respiratory failure caused by a fibrotic reaction1. It has long been suspected that the phagocytosis of silica by pulmonary macrophages induces the secretion of fibrogenic factors2. Several potentially fibrogenic cytokines released by macrophages have been identified, including interleukin-1 (IL-1) (ref. 3), tumour necrosis factor-α (TNF) (ref. 4), platelet-derived growth factor5, basic fibroblast growth factor6 and transforming growth factor-β (TGF-β) (ref. 7). Here we show that TNF plays an important part in silica-induced pulmonary fibrosis in mice in that (1) a single instillation of silica leads to a marked increase in the level of lung TNF messenger RNA which lasts for >70 days, while there are no obvious changes in the amounts of IL-lα or TGF-β mRNAs; and (2) silica-induced collagen deposition is almost completely prevented by anti-TNF antibody, but is significantly increased by continuous infusion of mouse recombinant TNF.
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Piguet, P., Collart, M., Grau, G. et al. Requirement of tumour necrosis factor for development of silica-induced pulmonary fibrosis. Nature 344, 245–247 (1990). https://doi.org/10.1038/344245a0
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DOI: https://doi.org/10.1038/344245a0
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