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)

72 cases of diffuse interstitial lung diseases were observed from 1969 to 1976. Specimens removed from 47 patients were subjected to the whole spectrum of reactions. According to variation of both elastin and collagen, the following groups were outlined: group A: mycobacteriosis, farmer's lung, sarcoidosis and silicosis; group B: chronic eosinophilic pneumonia, lymphocytic interstitial pneumonia, post-tuberculous pulmonary fibrosis, and group C: X-ray pneumopathy, desquamative interstitial pneumonia, sclerodermic pneumopathy and chronic pulmonary fibrosis (primary chronic fibroadenomyosis). Each of these groups presents a close relationship between histochemical, radiological, clinical and functional findings.
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PMID:Diffuse interstitial lung diseases: a histochemical approach. 623 29

Six months after intratracheal instillation of silica, histologic, ultrastructural, cytologic, and biochemical studies were performed on the lungs of guinea pigs. The tissue response consisted of both diffuse alveolar septal infiltration with interstitial fibrosis and granulomatous infiltration with nodular fibrosis. Ultrastructural studies confirmed the presence of a mixed inflammatory exudate in the alveolar interstitium (histiocytes, neutrophils, eosinophils, and lymphocytes) and the Type II lining of cell hyperplasia. The number of lung cells recovered by lavage and the proportions of neutrophils and multinucleated cells in bronchoalveolar cells were significantly greater in experimental animals (P < .05) than in controls (intratracheal saline). Total lung collagen and collagen synthesis by cultured lung tissue were also increased in the experimental animals. Since the response of guinea pig lung to intratracheal silica included pathologic features common to human silicosis and idiopathic pulmonary fibrosis, this model has the potential for improving our understanding of both of these important clinical disorders.
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PMID:Experimental silicosis: morphologic and biochemical abnormalities produced by intratracheal instillation of quartz into guinea pig lungs. 625 1

The authors induced pulmonary silicosis in albino rats by the intratracheal method with 50 mg mixed middling slime from Panaguiriste and quartz dust, dissolved in I ml physiological solution. The animals received a single treatment and were killed on 90th day of the experiment. Some intime characteristics of collagen-forming mechanisms in lungs were followed up via routine histological, histochemical, enzymohistochemical/ acid phosphatase activity, beta-glucoronidase, AS-esterase and lipase/ and autoradiographic/H3 labelled proline/ methods. It was established, that under the effect of both dusts from Panaguiriste mines studied/ mixed dust and pure quartz dust/ considerable deviations developed in the structure of the lungs of the experimental animals in the enzyme activity of acid phosphatase and carbon esterase, accompanied by various forms of fibrosis in the organ, depending on the dust applied. The difference in the composition of both dusts quartz and mixed dust slime - had an effect on the degree of the deviations, but not on their character, manifested in: I. specific protective reaction of organism, with activation of the ferments from the group of carbon esterase in macrophagic elements of interstitium and around the silicotic alterations in the lungs of the experimental animals; 2. inhibition of the maturation of macrophages in silicotic foci and 3. acceleration of the proliferation of fibroblasts with intensification of collagen-formation, accompanied by an enhanced activity of the ferments from the group of carbon esterase and in the cytoplasm of fibroblasts. The authors draw the conclusion that the complex use of routine histological, histochemical and quantitative isotope methods enables the more significant determination of fibrinogenicity of quartz-containing dust even at the early terms of their exposure under experimental conditions.
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PMID:[Histochemical mechanisms in etiology of pulmonary fibrosis after short-term exposure to a mixture of dust and quartz from copper mine]. 629 48

Pulmonary tissue obtained at thoracotomy or autopsy from 5 kaolin workers with complicated pneumoconiosis was studied by optical light and scanning electron microscopy. Premortem or preoperative chest roentgenograms demonstrated small irregular shadows and large opacities typical of kaolin pneumoconiosis. On gross examination, there were firm, grey-brown nodules and masses in the parenchyma and in the hilar lymph nodes. Histologically, there was extensive pulmonary kaolinite deposition associated with formation of peribronchiolar macules and nodules. The latter were comprised of kaolinite aggregates traversed by bands of fibrous tissue rather than dense whorled collagen, as seen in silicosis. Crystallographic studies confirmed the presence of kaolinite in the lungs, but silica was not demonstrable by either analytical scanning electron microscopy or X-ray diffractometry. These findings illustrate the pathology of human kaolin pneumoconiosis, confirm the fibrogenic potential of kaolinite, and emphasize differences in pulmonary responses to kaolinite and to silica.
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PMID:Kaolin pneumoconiosis. Radiologic, pathologic, and mineralogic findings. 646 82

Silicosis is usually attributed to fibroblast stimulation by secretion of damaged alveolar macrophages (AMs), but the role of polymorphonuclear leukocytes (PMNs) and of continuing cell injury in the pathogenesis has not been fully studied. Mice given intratracheal injections of 2 mg of silica received 3H-thymidine 1 hour before death at intervals to 20 weeks. Cellular populations and lysosomal content of lavage fluids were correlated with morphology, DNA synthesis, and collagen content of the lung. The initial response involved rapid PMN and AM recruitment to the alveoli. Some free particles crossed Type 1 epithelial cells, and silica was found in interstitial macrophages. Focal Type 1 cell damage was rapidly repaired by Type 2 cell proliferation. Although PMN numbers dropped after a few days, they never reached control levels and rose again after 8 weeks; the number of AMs fell to control values from 2 to 8 weeks, then increased again. Glucosaminidase and glucuronidase levels in the lavage fluid were much higher than control levels throughout the study. Increased DNA synthesis by interstitial cells occurred from 2 days to 20 weeks; increased collagen synthesis was found from 4 weeks onward. The continuing inflammatory response of the lung to silica suggests may contribute to fibroblastic stimulation.
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PMID:Role of polymorphonuclear leukocytes in silica-induced pulmonary fibrosis. 648 44

Early diagnosis of lung fibrosis has been hampered by the lack of a simple, convenient and specific method. Recently Rohde et al. developed an assay method for Type III procollagen peptide. Type III procollagen peptide, an extension peptide released during the biosynthesis of collagen Type III, has been known as a good marker for hepatic fibrosis. Therefore, we applied this assay to the patients with idiopathic pulmonary fibrosis, lung fibrosis in collagen disease and silicosis. And also we measured the serum level of the peptide in the healthy workers being exposed to silica. Normal value of the peptide in adults was 8.3 +/- 2.6 (mean +/- SD; n = 32) ng/ml. The upper value over mean + 2SD, 13.4 ng/ml, was regarded as abnormal value. Six patients with idiopathic pulmonary fibrosis, and lung fibrosis in collagen disease showed a significant increased level of 19.0 +/- 9.6 ng/ml (P less than 0.02). Four of 6 patients had abnormal high values. On the other hand, the patients with silicosis had not so high levels of peptide (12.6 +/- 6.5 ng/ml; n = 24; P less than 0.01), but 25% of the patients showed abnormal values. There were 2 cases among 19 healthy workers being exposed to silica who revealed slight abnormal values, 15.6 and 16.7 ng/ml. These observations suggest that the assay has a prognostic value for lung fibrosis and also is useful for the early detection of active lung fibrosis in the workers, even though Type III procollagen biosynthesis is already low in the late stages of silicosis.
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PMID:[Serum type III procollagen peptide in patients with pneumoconiosis]. 667 53

It was proved in this experiment that tetrandrine, one of the bisbenzylisoquinoline alkaloids, may inhibit the development of experimental silicosis on rats whether the drug was given to the animal right after dusting or after the formation of silicotic nodules. As compared to the silicotic control rats, lowering of total weight and collagen content of the lungs were shown and some degradation of collagen fibers was also indicated from the histopathological examination.
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PMID:Observation of the effect of tetrandrine on experimental silicosis of rats. 687 15

During the last 10 years our investigations have confirmed that collagen is not the major protein material in the lesions of progressive massive fibrosis of coal workers. In previous studies it was demonstrated that a substance similar in composition to fibrin was an important component in these masses. We report immunohistochemical studies on the lungs of seven coalworkers which show that the complex extracellular material in six of the lesions of massive fibrosis contains fibronectin. Preliminary observations indicate that fibronectin is also present in the lesions of silicosis and asbestosis.
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PMID:Presence of fibronectin in pneumoconiotic lesions. 704 22

The acute inflammatory reaction in the lungs of guinea pigs produced by the intratracheal injection of silica was assessed by histologic studies and whole-lung lavage 1, 2, 4, 7, and 14 days after the intratracheal instillation of quartz particles or saline. In addition, lavaged macrophages were cultured in vitro, and the media were assayed for chemotactic factors. This exposure to silica produced a neutrophilic inflammatory response around terminal bronchioles that was well developed within 1 day after injection. Four days after injection, neutrophils were replaced by mononuclear cells; and by 7 days, loosely organized granulomas and collagen deposition were detected in the interstitium. The number of neutrophils (PMNs) recovered by lavage from experimental animals was greatest 1 day after injection and was significantly greater (P less than 0.01) than that for controls at all time points. In contrast, the number of macrophages recovered by lavage did not exceed control levels until 7 days after injection and remained elevated thereafter. Thus, the cells recovered by lavage tended to mirror the changes seen in the inflamed lung. In experiments utilizing blind-well chemotactic chambers, both peritoneal exudate neutrophils and macrophages migrated toward supernatants from cultures of alveolar macrophages lavaged from silica-exposed animals in greater numbers (P less than 0.02) than toward supernatant from control animal macrophage cultures at each time point. Migration of normal alveolar macrophages toward supernatants from all cultures was minimal. Thus, exposure to silica in vivo appears to be a potent stimulus for the release of neutrophil and monocyte chemotactic factors by alveolar macrophages in vitro. The correlation between the types of inflammatory cells identified in the lung both microscopically and by lavage and the chemotactic factors released in vitro by alveolar macrophages from these lungs suggests that alveolar macrophages play a role in mediating pulmonary inflammation in this form of experimental silicosis.
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PMID:Acute experimental silicosis. Lung morphology, histology, and macrophage chemotaxin secretion. 712 6

Intratracheal instillation of bleomycin (0.08 U) or silica (2 mg) to mice leads, after 15 days, to a patchy pulmonary fibrosis associated with a significant increase of the lung hydroxyproline. Since tumour necrosis factor (TNF) seems to be an important mediator in pulmonary fibrosis, we wondered whether this fibrosis might be prevented by a new TNF-alpha antagonist. Infusion of a 55 kD human recombinant soluble TNF receptor rsTNFR-beta, at a rate of 20 micrograms.day-1, prevented the bleomycin/silica induced increase of lung hydroxyproline content, as measured 15 days after instillation. Infusion of rsTNFR-beta was also effective in the treatment of an established fibrosis, i.e. administered 25 or more days after instillation of bleomycin or silica, since it reduced lung collagen content. Recombinant soluble TNFR-beta had no significant influence on the number of cells, mostly macrophages, recovered by bronchoalveolar lavage. The examination of histological sections indicated that the rsTNFR-beta reduced the proportion of areas of damaged lung and, in silicosis, the formation of nodules with a rich collagen content. This study suggests that rsTNFR-beta might be useful in the therapy of pulmonary fibrosis.
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PMID:Treatment by human recombinant soluble TNF receptor of pulmonary fibrosis induced by bleomycin or silica in mice. 801 95


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