Literature DB >> 2692694

Inflammatory responses in lungs of rats inhaling coalmine dust: enhanced proteolysis of fibronectin by bronchoalveolar leukocytes.

G M Brown1, K Donaldson.   

Abstract

Chronic exposure to coalmine dust is associated with the accumulation of inflammatory leukocytes in the bronchoalveolar region of the lung and, in the long term, with fibrosis and emphysema of the lung parenchyma. Degradation of connective tissue by inflammatory leukocytes has been implicated in the parenchymal damage that precedes the development of fibrotic or emphysematous lesions in the lung. The ability of inflammatory leukocytes obtained by bronchoalveolar lavage from rats inhaling coalmine dust to degrade fibronectin in vitro was assessed. The animals were exposed to an airborne mass concentration of dust similar to the maximum permissible level in United Kingdom collieries. The bronchoalveolar lavage cell population showed changes with duration of dust exposure; there were increases in the total number of leukocytes and in the percentage of polymorphonuclear leukocytes, and the macrophage component of the lavage became increasingly activated, as assessed by the ability of these cells to spread on glass. In addition, degradation of a radiolabelled fibronectin matrix by the coalmine dust exposed bronchoalveolar leukocytes increased with duration of dust exposure. Thus exposure to airborne coalmine dust causes an influx of inflammatory leukocytes to the alveolar region. These cells have enhanced ability to degrade fibronectin and this may be important in subsequent disease development.

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Year:  1989        PMID: 2692694      PMCID: PMC1009884          DOI: 10.1136/oem.46.12.866

Source DB:  PubMed          Journal:  Br J Ind Med        ISSN: 0007-1072


  31 in total

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Journal:  Biochem J       Date:  1984-09-15       Impact factor: 3.857

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Journal:  J Clin Invest       Date:  1987-01       Impact factor: 14.808

6.  Kinetics of inflammatory and fibrotic pulmonary changes in a murine model of silicosis.

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Journal:  Am Rev Respir Dis       Date:  1985-05

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Journal:  Am Rev Respir Dis       Date:  1985-08

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Journal:  Exp Lung Res       Date:  1986       Impact factor: 2.459

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  7 in total

Review 1.  Coal mining and chronic obstructive pulmonary disease: a review of the evidence.

Authors:  D Coggon; A Newman Taylor
Journal:  Thorax       Date:  1998-05       Impact factor: 9.139

2.  Length-dependent retention of carbon nanotubes in the pleural space of mice initiates sustained inflammation and progressive fibrosis on the parietal pleura.

Authors:  Fiona A Murphy; Craig A Poland; Rodger Duffin; Khuloud T Al-Jamal; Hanene Ali-Boucetta; Antonio Nunes; Fiona Byrne; Adriele Prina-Mello; Yuri Volkov; Shouping Li; Stephen J Mather; Alberto Bianco; Maurizio Prato; William Macnee; William A Wallace; Kostas Kostarelos; Ken Donaldson
Journal:  Am J Pathol       Date:  2011-06       Impact factor: 4.307

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Authors:  A Seaton
Journal:  Br J Ind Med       Date:  1990-07

4.  Longitudinal and cross sectional analyses of exposure to coal mine dust and pulmonary function in new miners.

Authors:  N S Seixas; T G Robins; M D Attfield; L H Moulton
Journal:  Br J Ind Med       Date:  1993-10

5.  Quantitative relation between emphysema and lung mineral content in coalworkers.

Authors:  J Leigh; T R Driscoll; B D Cole; R W Beck; B P Hull; J Yang
Journal:  Occup Environ Med       Date:  1994-06       Impact factor: 4.402

6.  No association between pyrite content and lung cell responses to coal particles.

Authors:  Graeme R Zosky; Ellen J Bennett; Macarena Pavez; B Basil Beamish
Journal:  Sci Rep       Date:  2021-04-14       Impact factor: 4.379

Review 7.  Minerals, fibrosis, and the lung.

Authors:  A G Heppleston
Journal:  Environ Health Perspect       Date:  1991-08       Impact factor: 9.031

  7 in total

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