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Expression and Localization of TIMP‐1, TIMP‐2, MMP‐13, MMP‐2, and MMP‐9 in Early and Advanced Experimental Lung Silicosis

Chronic exposure to crystalline silica particles results in macrophagelymphocytic granulomatous lung inflammation, which is followed by abnormal and progressive accumulation of extracellular matrix. 1,2 However, the pathogenic mechanisms and the sequence of the pathological events leading to the fibrotic response have not been well defined. In this context, there is evidence suggesting an upregulation of a variety of fibrogenic cytokines such as tumor necrosis factor alpha (TNFα ) and transforming growth factor beta (TGFβ ), with increased synthesis and secretion of lung extracellular matrix components. 3,4 However, studies on matrix degradation are scanty.