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  • 1
    Electronic Resource
    Electronic Resource
    Elevated interleukin-8 in the alveolitis of individuals with asbestos exposure (1996)
    Springer
    International archives of occupational and environmental health 68 (1996), S. 109-114 
    Details
    ISSN: 1432-1246
    Keywords: Key words Asbestos exposure ; Neutrophils ; Interleukin-8
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Asbestosis is a fibrotic and inflammatory interstitial lung disease occurring after chronic occupational exposure to asbestos. An alveolitis has been described with activated alveolar macrophages and increased neutrophils as sampled by bronchoalveolar lavage (BAL). Animal models and in vitro studies demonstrate that asbestos can stimulate alveolar macrophages to release neutrophil chemotactic factor. We performed BAL on 18 nonsmoking individuals with asbestos exposure and observed a twofold increase in percent neutrophils recovered. Alveolar macrophages cultured in vitro from the asbestos-exposed individuals spontaneously released significant amounts of the neutrophil chemotaxin, interleukin-8 (IL-8). In addition, the alveolar macrophages expressed a 2.7-fold increase in steady state mRNA levels compared to unexposed normal controls utilizing the reverse transcriptase/polymerase chain reaction. In vitro experiments confirmed that crocidolite or chrysotile asbestos could stimulate the release of IL-8 from mononuclear phagocytes in a dose-dependent fashion. We conclude that asbestos exposure causes a mild neutrophilic alveolitis, and that IL-8 is one potential mediator capable of contributing to this inflammation in the lower respiratory tract.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00381242
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  • 2
    Electronic Resource
    Electronic Resource
    Angular and fibrous particles in lung in relation to silica-induced diseases (1998)
    Springer
    International archives of occupational and environmental health 71 (1998), S. 263-269 
    Details
    ISSN: 1432-1246
    Keywords: Key words Angular and fibrous particles ; Silica ; Lung cancer ; TEM-EDS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Introduction: The lung concentration of angular and fibrous particles was measured in cases of lung fibrosis only, in cases of lung fibrosis and lung cancer, and in cases of lung cancer only. These patients worked in different trades (mining, foundries, construction and were not a homogeneous group of exposed workers. Material and methods: Particles, both angular and fibrous, were extracted from lung parenchyma by a bleach digestion method, mounted on copper microscopic grids by a carbon replica technique, and analyzed by transmission electron microscopy (TEM) and energy-dispersive spectroscopy (EDS). The quartz concentration was also determined by X-ray diffraction (XRD) on a silver membrane filter after extraction from the lung parenchyma. Results: (1) Lung cancer and lung fibrosis cases retained more metal-rich particles (P=0.02) and more angular particles of all sorts (P=0.009) than did lung fibrosis cases only, and the differences were statistically significant. (2) However, more quartz was retained in the lungs in lung fibrosis cases than in lung fibrosis or lung cancer cases, but the difference in the concentrations was not statistically significant. (3) More ferruginous bodies were retained in the lungs in lung cancer and lung fibrosis cases than in cases of lung fibrosis only, and the difference in the concentrations was statistically significant (P=0.02). Conclusion: Results obtained from lung tissue must always be interpreted cautiously. However, these results are consistent with the hypothesis that workers in some trades such as foundries were exposed not only to quartz but also to asbestos, ceramic fibers, metal-rich non fibrous particles, and other likely carcinogenic chemicals. The wide range of particle types identified in the lungs of these workers illustrates the complexity of trying to determine disease origins in these work environments. Epidemiology studies have to control for the exposure to these carcinogens as well as for smoking habits.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004200050279
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Immunohistochemical localization of transforming growth factor-β and insulin-like growth factor-I in asbestosis in the sheep model (1997)
    Springer
    International archives of occupational and environmental health 69 (1997), S. 157-164 
    Details
    ISSN: 1432-1246
    Keywords: Key words Insulin-like growth factor I ; Transforming ; growth factor-β ; Pulmonary fibrosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Asbestosis is characterized by increased collagen deposition along the walls of terminal respiratory bronchioles that extends into the alveolar ducts and septae. Alveolar macrophages are activated and release growth factors that stimulate mesenchymal cell proliferation and enhanced formation of extracellular matrix. Both insulin-like growth factor-I (IGF-I), and transforming growth factor β (TGF-β) regulate cellular growth and promote matrix accumulation and are hypothesized to play important roles in asbestosis. We performed immunohistochemistry using polyclonal antibodies to specific synthetic peptides of the three mammalian isoforms of TGF-β (TGF-β1, -β2, -β3) and to IGF-I on lungs of sheep treated intratracheally with chrysotile asbestos. All three TGF-β isoforms were found in bronchial and bronchiolar epithelium, macrophages, and bronchial and vascular smooth muscle in control lungs. The distribution of TGF-β was increased in these lung constituents as fibrotic lesions developed. Fibrotic lesions additionally demonstrated intense immunostaining of all three TGF-β isoforms that localized to the extracellular matrix zones with little staining of interstitial cells. In the control sheep lungs, IGF-I staining was detected in bronchial and bronchiolar epithelium, bronchial glands, bronchial and vascular smooth muscle, endothelium, and macrophages. IGF-I immunostaining was detected in macrophages in peribronchial fibrosis and in fibroblasts along the periphery of and within lesions, but not in the extracellular matrix. Metaplastic proliferating epithelium and macrophages were strongly immunoreactive for IGF-I in advanced lesions. Our data demonstrate different immunostaining patterns for IGF-I and TGF-β in asbestosis, with IGF-I in the cellular periphery and TGF-β in the extracellular matrix consistent with a complementary role in stimulating interstitial fibroblast proliferation and new collagen deposition in areas of active fibrosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004200050132
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  • 4
    Electronic Resource
    Electronic Resource
    Isoniazid Levels in the Bronchoalveolar Lavage Fluid of Patients with Pulmonary Tuberculosis (1998)
    Springer
    Lung 176 (1998), S. 205-211 
    Details
    ISSN: 1432-1750
    Keywords: Key words: Isoniazid—Bronchoalveolar lavage fluid.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Isoniazid (INH) is one of the most important first line drugs in the treatment of tuberculosis. We utilized high performance liquid chromatography with a hydrazone extraction technique to measure INH in bronchoalveolar lavage (BAL) fluid specimens from six patients with active pulmonary tuberculosis. We found BAL fluid INH levels to be similar to 2-h peak serum levels. The concentration of INH in BAL fluid from lobes with infiltrate was similar to the concentration of INH in BAL fluid from lobes without infiltrate (0.062 μg/ml and 0.073 μg/ml, respectively). After adjusting for protein concentration in the BAL fluid, INH levels in lobes with infiltrate were threefold lower than in lobes without infiltrate. The correlation between the concentration of INH in serum and BAL fluid approached significance after correcting for protein (lobes with infiltrate, r 2= 0.60 (p= 0.07); lobes without infiltrate, r 2= 0.50 (p= 0.12)). INH penetrates into bronchoalveolar fluid, and concentrations of INH in the BAL fluid suggest that assessment of the INH serum concentration is adequate to evaluate bioavailability of the drug in patients with pulmonary tuberculosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00007603
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    The Gene for Lysosomal Protein CD63 Is Normal in Patients with Hermansky-Pudlak Syndrome (1998)
    Springer
    Lung 176 (1998), S. 249-256 
    Details
    ISSN: 1432-1750
    Keywords: Key words: Hermansky-Pudlak syndrome—CD63—Granulophysin.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Hermansky-Pudlak syndrome (HPS) is one of the few genetic disorders associated with severe pulmonary fibrosis. Fifty percent of affected patients die as a result of respiratory insufficiency. Fibrosis is thought to be caused by the accumulation of ceroid, an insoluble fluorescent lipoprotein, both extracellularly and in the lysosomes of alveolar macrophages. In addition to pulmonary fibrosis, HPS is characterized by oculocutaneous albinism and a reduction in the number of platelet dense bodies. CD63 is a protein that was described originally in platelet lysosomes. It localizes to the membranes of melanosomes and platelet dense bodies. CD63 is decreased dramatically in the lysosomes and dense bodies of patients with HPS. We theorized that CD63, a membrane protein common to lysosomes, melanosomes, and platelet dense bodies, may play a role in HPS. We sought to characterize the gene coding for this protein in HPS lymphoid cell lines. The coding region for CD63 was sequenced in control and HPS cell lines. Messenger RNA from HPS and normal cell lines was examined by Northern analysis. Genomic DNA from the same cell lines was examined by Southern analysis and polymerase chain reaction (PCR). CD63 protein in lymphoid cell lines and peripheral blood monocytes was compared by Western analysis. We found no mutations in the coding region of CD63 in an HPS cell line. We also found no diminution in the quantity of CD63 RNA by Northern analysis and no gross defects in the structural gene by PCR and Southern analysis, suggesting that the CD63 structural gene, promoter, and untranslated regions were normal. Western analysis showed that the 43-kDa protein was present in control and HPS lymphoid cell lines and peripheral blood monocytes in equivalent amounts. Although CD63 is an attractive candidate for the primary defect of HPS, the disease is probably not caused by a mutation in the CD63 gene.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00007607
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    Paper (German National Licenses)
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