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

The dynamic mechanical properties of lung tissue and its contents of collagen and elastic fibers were studied in strips prepared from mice instilled intratracheally with saline (C) or silica [15 (S15) and 30 days (S30) after instillation]. Resistance, elastance, and hysteresivity were studied during oscillations at different frequencies on S15 and S30. Elastance increased from C to silica groups but was similar between S15 and S30. Resistance was augmented from C to S15 and S30 and was greater in S30 than in S15 at higher frequencies. Hysteresivity was higher in S30 than in C and S15. Silica groups presented a greater amount of collagen than did C. Elastic fiber content increased progressively along time. This increment was related to the higher amount of oxytalan fibers at 15 and 30 days, whereas elaunin and fully developed elastic fibers were augmented only at 30 days. Silicosis led not only to pulmonary fibrosis but also to fibroelastosis, thus assigning a major role to the elastic system in the silicotic lung.
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PMID:Lung tissue mechanics and extracellular matrix composition in a murine model of silicosis. 1124 40

Silica has been reported to directly stimulate cellular proliferation of human lung fibroblasts, and silica-treated macrophage supernatants induce fibroblast proliferation and some of their biosynthetic activities. Alveolar macrophages produce increased amount of tumour necrosis factor alpha (TNF-alpha) and transforming growth factor beta (TGF-beta). Lung fibroblasts are producers of interleukin-6 (IL-6). We investigated the capacity of lung fibroblasts obtained from normal and silicosis subjects to elaborate IL-6 in response to TNF-alpha and to TGF-beta. Our data show that TNF-alpha and TGF-beta are able to stimulate the proliferation of human lung fibroblasts in culture, to increase the collagen production of the cells and are both able to increase IL-6 production by lung fibroblasts of patients with silicosis. We hypothesise that silica is able to stimulate lung fibroblast both directly, increasing the cell proliferation, and indirectly stimulating the release of factors (as TNF-alpha and TGF-beta) from activated alveolar macrophages, that are able to increase proliferative and biosynthetic activities of fibroblast.
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PMID:Effects of silica on human lung fibroblast in culture. 1132 86

We investigated the role of Fas ligand in murine silicosis. Wild-type mice instilled with silica developed severe pulmonary inflammation, with local production of tumor necrosis factor (TNF)-alpha, and interstitial neutrophil and macrophage infiltration in the lungs. Strikingly, Fas ligand-deficient generalized lymphoproliferative disease mutant (gld) mice did not develop silicosis. The gld mice had markedly reduced neutrophil extravasation into bronchoalveolar space, and did not show increased TNF-alpha production, nor pulmonary inflammation. Bone marrow chimeras and local adoptive transfer demonstrated that wild-type, but not Fas ligand-deficient lung macrophages recruit neutrophils and initiate silicosis. Silica induced Fas ligand expression in lung macrophages in vitro and in vivo, and promoted Fas ligand-dependent macrophage apoptosis. Administration of neutralizing anti-Fas ligand antibody in vivo blocked induction of silicosis. Thus, Fas ligand plays a central role in induction of pulmonary silicosis.
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PMID:Fas ligand triggers pulmonary silicosis. 1145 90

While silica particles are considered to be fibrogenic and carcinogenic agents, the mechanisms responsible are not well understood. This article summarizes literature on silica-induced accelerated silicosis, chronic silicosis, silico-tuberculosis, bronchogenic carcinoma, and immune-mediated diseases. This article also discusses the generation of reactive oxygen species (ROS) that occurs directly from the interaction of silica with aqueous medium and from silica-stimulated cells, the molecular mechanisms of silica-induced lung injuries with focus on silica-induced NF-kappaB activation, including its mechanisms, possible attenuation and relationship to silica-induced generation of cyclooxygenase II and TNF-alpha. Silica-induced AP-1 activation, protooncogene expression, and the role of ROS in these processes are also briefly discussed.
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PMID:Diseases caused by silica: mechanisms of injury and disease development. 1181 22

We investigated immunopathogenic roles for apoptosis in acute murine silicosis. Intratracheal silica instillation induced pulmonary inflammation and enlarged thoracic lymph nodes. Lymphocytes from silica-exposed lymph nodes showed reduced mitogenic responses to T cell receptor (TCR) stimulation, and markedly increased activation-induced cell death, compared with control lymphocytes from saline-exposed lymph nodes. CD4(+) T cell death was mediated by Fas ligand, because CD4(+) T cells from Fas ligand-deficient gld mice did not undergo activation-induced apoptosis. Silica deposition also resulted in increased apoptosis associated with inflammatory infiltrates in lung parenchyma. In vivo treatment with caspase inhibitors reduced neutrophil accumulation, and alleviated inflammation in the lungs of silica-treated mice. These results suggest that silica-induced apoptosis plays an inflammatory role in the lung parenchyma, and creates immunologic abnormalities in regional lymph nodes, with pathogenic implications for the host.
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PMID:Apoptosis underlies immunopathogenic mechanisms in acute silicosis. 1209 Dec 49

Macrophages play a fundamental role in silicosis in part by removing silica particles and producing inflammatory mediators in response to silica. Tumor necrosis factor alpha (TNFalpha) is a prominent mediator in silicosis. Silica induction of apoptosis in macrophages might be mediated by TNFalpha. However, TNFalpha also activates signal transduction pathways (NF-kappaB and AP-1) that rescue cells from apoptosis. Therefore, we studied the TNFalpha-mediated mechanisms that confer macrophage protection against the pro-apoptotic effects of silica. We will show that exposure to silica induced TNFalpha production by RAW 264.7 cells, but not by IC-21. Silica-induced activation of NF-kappaB and AP-1 was only observed in RAW 264.7 macrophages. ERK activation in response to silica exposure was only observed in RAW 264.7 macrophages, whereas activation of p38 phosphorylation was predominantly observed in IC-21 macrophages. No changes in JNK activity were observed in either cell line in response to silica exposure. Silica induced apoptosis in both macrophage cell lines, but the induction of apoptosis was significantly larger in IC-21 cells. Protection against apoptosis in RAW 264.7 cells in response to silica was mediated by enhanced NF-kappaB activation and ERK-mediated phosphorylation of the p55 TNFalpha receptor. Inhibition of these two protective mechanisms by specific pharmacological inhibitors or transfection of dominant negative mutants that inhibit IkappaBalpha or ERK phosphorylation significantly increased silica-induced apoptosis in RAW 264.7 macrophages. These data suggest that NF-kappaB activation and ERK-mediated phosphorylation of the p55 TNF receptor are important cell survival mechanisms in the macrophage response to silica exposure.
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PMID:Phosphorylation of tumor necrosis factor receptor 1 (p55) protects macrophages from silica-induced apoptosis. 1457 Aug 68

Approximately 90% of freshly imported macaques and other Old World Monkeys are known to be infected with respiratory mites. The lung associated pigments are integral components of pulmonary acariasis in Old World Monkeys; at least three distinctive pigmental bodies are identified in association with lung mite infection. Two major components of pigments are recently identified as silica by using elemental analysis using a high voltage electron microscope and an energy-dispersive X-ray analysis technique. Since a limited number of infected monkey lung tissues and associated pigments can be examined by this tedious procedure, it was important for us to examine much greater number of specimens to verify our initial observation. Ten microincineration technique described provided a unique and practical way to identify the mineral elements in as many 27 histologic sections within a short span of time. Silica and silicates are heat resistant whereas majority of organic materials including lung mite parasites disintegrated under the extreme temperature. Mineral elements were exclusively located within the polarizable white ash. More than 90% of total pigmental bodies identified were found to be related to siliceous materials in 20 incinerated infected monkey lung tissues whereas five noninfected lungs similarly examined did not reveal any pigmental bodies. Other than a small of fine granular mucin substances which were PAS positive, the majority of lung mite associated pigments such as large granules of hemosiderin, needle-like crystals and other fine granules engulfed by macrophages were identified to be siliceous materials as they have persisted even after microincineration. Mite parasites and other organic materials were completely disintegrated. Similar pigmental bodies examined by microscope X-ray analysis were positive for silicate. This finding suggests that lung mite infection in Old Monkeys apparently predisposed silicosis. Therefore, until the link between lung mite infection and silicosis is clarified, experimental inhalation toxicologic findings in mite-infected Old World monkeys should be interpreted cautiously.
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PMID:A histologic demonstration of siliceous materials in simian lung mite infected lung tissues by microincineration. 1461 Mar 63

In an examination of the relationship between silicosis and lung function, relevant studies of silica-exposed workers were reviewed. Smoking, dust exposure, and emphysema are three important factors that can confound the association between silicosis and lung function. Despite the importance of smoking in relation to lung function, some studies did not control for smoking, or smoking was controlled inadequately. The data suggest a weak association between lung function (mainly obstruction) and dust exposure, although some studies had crude measures of exposure. In general, the lung function of those with radiographic silicosis in category 1 was indistinguishable from those in category 0. Those in category 2 had small reductions in lung function relative to those with category 0 and little difference in the prevalence of emphysema. There were slightly greater decrements in lung function with category 3 and more significant reductions with progressive massive fibrosis. Emphysema was related to higher categories of silicosis, as well as to smoking. Silica exposure was often inadequately controlled in studies examining silicosis and lung function. A few studies suggested that emphysema is an independent risk factor associated with significant reductions in lung function.
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PMID:Relationship between silicosis and lung function. 1501 24

It is estimated that about 4% of cancer mortality is attributed to occupational risk factors. Due to long latency periods it is often difficult to establish causal relationships. Thoracal cancer accounts for about 88% of all compensated occupational cancers in Germany. Most important exposures and diseases are asbestos-related lung cancer, asbestos-related malignant mesothelioma and radiation induced lung cancer (by Radon and its decay products). Lung cancer caused by nickel compounds, hexavalent chromium, arsenic and its compounds, coke oven gases and polycyclic aromatic hydrocarbons are rare. Silica-dust induced lung cancer can be compensated as occupational disease if a silicosis is present. In Germany every physician is obliged to notify a suspected occupational cancer as well as other occupational diseases.
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PMID:[Occupation related thoracic tumors]. 1510 80

India being a developing nation is faced with traditional public health problems like communicable diseases, malnutrition, poor environmental sanitation and inadequate medical care. However, globalization and rapid industrial growth in the last few years has resulted in emergence of occupational health related issues. Agriculture (cultivators i.e. land owners + agriculture labourers) is the main occupation in India giving employment to about 58% of the people. The major occupational diseases/morbidity of concern in India are silicosis, musculo-skeletal injuries, coal workers' pneumoconiosis, chronic obstructive lung diseases, asbestosis, byssinosis, pesticide poisoning and noise induced hearing loss. There are many agencies like National Institute of Occupational Health, Industrial Toxicology Research Centre, Central Labour Institute, etc. are working on researchable issues like Asbestos and asbestos related diseases, Pesticide poisoning, Silica related diseases other than silicosis and Musculoskeletal disorders. Still much more is to be done for improving the occupational health research. The measures such as creation of advanced research facilities, human resources development, creation of environmental and occupational health cells and development of database and information system should be taken.
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PMID:Occupational health research in India. 1512 63


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