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Query: UMLS:C0037116 (silicosis)
 1,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 reaction. It has long been suspected that the phagocytosis of silica by pulmonary macrophages induces the secretion of fibrogenic factors. Several potentially fibrogenic cytokines released by macrophages have been identified, including interleukin-1 (IL-1), tumour necrosis factor-alpha (TNF), platelet-derived growth factor, basic fibroblast growth factor and transforming growth factor-beta (TGF-beta). 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 greater than 70 days, while there are no obvious changes in the amounts of IL-1 alpha or TGF-beta 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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PMID:Requirement of tumour necrosis factor for development of silica-induced pulmonary fibrosis. 215 65

Silicosis is a chronic lung disease, which is caused by inhalation of silica-containing dusts, leading to pulmonary fibrosis. Alveolar macrophages play a key-role in defence against these particles entering the lung. As a result of phagocytosis, the macrophages release mediators, which are involved in various processes of inflammation and immunological defence mechanisms. We established an in-vitro test system composed of human macrophages, human pneumocyte type II cells (line A-549), human diploid lung fibroblasts (line Wi38) and human tracheobronchial epithelial cells (line BEAS-2B). With this model, we were able to study the influence of various cytokines, produced by the macrophages, on cell proliferation and collagen synthesis (only fibroblasts) of the cells in our test-system. In this report, we will summarize data obtained from our in-vitro test system on two cytokines, which are thought to be important in pathogenesis of lung fibrosis: insulin-like growth factor-1 (IGF-1) and transforming growth factor-beta (TGF-beta).
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PMID:Supernatants from quartz dust treated human macrophages stimulate cell proliferation of different human lung cells as well as collagen-synthesis of human diploid lung fibroblasts in vitro. 982 Jun 52

Excessive exposure to respirable particles of crystalline silica is an occupational health problem in developing countries and can cause a variety of pulmonary diseases, such as silicosis, chronic obstructive pulmonary disease (COPD), and malignancy, in susceptible hosts. In addition to the well-documented role of pulmonary macrophages, lymphocytes occasionally have been suggested to influence the pneumoconiotic process, but their potential role is not clearly understood. Interferon-gamma (IFN-gamma), a lymphocyte cytokine, is recognized as the most important cytokine in converting macrophages from a resting to an activated state. The aim of the present study was to investigate serum IFN-gamma levels and pulmonary function changes in silica-exposed workers and in silicosis. Twenty-seven silica workers (aged 35.6 +/- 8.2 years with 5.11 +/- 2.98 years exposure duration) and 18 unexposed office workers (aged 33.8 +/- 12 years) were included in the study. Mean spirometry parameters and smoking history were comparable to the values of the office workers, but COPD prevalence was higher in the silica-exposed group, and the age-adjusted ratio was more sensitive than fixed quotient criteria for airway obstruction. We found silicosis in 4 silica workers. The mean serum IFN-gamma level was increased in silica-exposed workers (10.22 +/- 22.68 pg/mL) although it was undetectable in all office workers and even in the workers with silicosis. Evaluating pulmonary function tests (PFT) using an age-adjusted quotient may prevent underestimation of airflow limitation, especially in the young population with risk factors. Although serum IFN-gamma may increase initially in response to silica, low levels of IFN-gamma in later stages may be considered a risk factor for silicosis because this cytokine downregulates the fibroblast responses to transforming growth factor-beta (TGF-beta) and decreases collagen production. Additional research to determine the exact role of this potent cytokine may offer insight into the pathogenesis of silicosis.
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PMID:Lung function and IFN-gamma levels in the sera of silica-exposed workers. 1854 61