Silicosis: Pathogenesis and Biomarkers - Abstract
Ramazzini first described this disease, namely “Pneumonoultramicroscopicsilicovolcanokoniosis” and then was changed according to the types of exposed dust. No reliable figures on the silicainhalation exposed individuals are officially documented. How silica particles stimulate pulmonary response and the exact path physiology of silicosis are still not known and urgently require further research. Nevertheless, many researchers hypothesized that pulmonary alveolar macrophages play a major role by secreting fibroblast-stimulating factor and re-ingesting these ingested silica particles by the pulmonary alveolar macrophage with progressive magnification. Finally, ending up of the death of the pulmonary alveolar macrophages and the development of pulmonary fibrosis appear. Various mediators, such as CTGF, FBRS, FGF2/bFGF, and TNF? play a major role in the development of silica-induced pulmonary fibrosis. A hypothesis of silicosis-associated abnormal immunoglobulins has been postulated. In conclusion, novel studies on pathogenesis and biomarkers of silicosis are urgently needed for precise prevention and control of this silently threaten disease of the world.