Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037116 (silicosis)
 1,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the bronchial mucus of patients with long-term airway obstruction free elastolytic activities are observed. These originate from leucocytes with polymorphous nuclei and may cause the digestion of lung tissue and thus an emphysematous lung metaplasia. It is known that the supersensitivity of bronchial musculature increases due to the influence of proteolytic ferments. For the inhibition of elastolytic enzymes, specific, acid-proof, low-molecular inhibitory substances are available. We were able to measure three of them in bronchial mucus against different substrates; i.e. against substrates for trypsin, pancreas elastase and leucocyte elastase. Our results show that the free inhibitor preparation decreases if free elastolytic activity in bronchial mucus is measured and is no longer available if the concentration decreases. It was also found that the concentration of secretory IGA decreases if the elastolytic activity increases. Thus, it is possible that the secretory IGA molecule is attacked by proteolytic enzymes. It is known that in case of chronic obstructive airway diseases lysozyme is released from leucocytes with polymorphous nuclei; in case of silicosis, from macrophages as well. In this study, the lysozyme concentration served as measurement for cell decomposition. The observation showed that in spite of the same lysozyme levels the elastolytic activity in patients can be very different. It is in strong connection with the available inhibitor capacity. Regarding the clinical evaluation can be concluded that some patients show a lack of secretory inhibitors. On a long-term basis, this lack can lead to the formation of emphysemata.
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PMID:Inhibitor activity against elastolytic enzymes in the bronchial area. A contribution to the pathogenesis of chronic airway obstruction. 385 11

To investigate the role of mast cells (MC) and their fibrogenic growth factors in silicosis, we performed quantitative immunohistochemistry for MC tryptase and for basic fibroblast growth factor (bFGF) in lung tissue from silicotic and control subjects. Anti-bFGF antibody was bound to lung MC, basement membrane, endothelial cells, and smooth-muscle cells. Morphometric analysis revealed that the volume density (V(v)) of MC was increased in silicotic lung and that the V(v) of bFGF-positive (bFGF(+)) cells was significantly higher than normal in silicotic lung. Most MC contained bFGF (rho = 0.88, p < 0.001). The V(v) of collagen/reticulin fibers was increased in silicosis and correlated with the V(v) of bFGF(+) cells (rho = 0.81, p < 0.001). Immature silicotic nodules contained bFGF(+) MC throughout the loose array of collagen/reticulin fibers. In large, mature nodules, the density of collagen/reticulin fibers was higher, and bFGF(+) MC were found only in the nodule periphery. Because of this circumferential MC alignment in silicotic nodules, we observed a negative correlation between the V(v) of bFGF(+) MC and the density of collagen/reticulin fibers in silicotic nodules (rho = -0.80, p < 0.001) and between the V(v) of all other nodule-associated cells and the density of collagen/reticulin fibers in the hypocellular nodule centers (rho = -0.84, p < 0.001). We conclude that MC that produce bFGF may play an important role in the development of silicosis.
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PMID:Mast cell basic fibroblast growth factor in silicosis. 1085 84