Abstract
Pneumoconiosis is the world’s most common disease caused by the inhalation of dust. Pneumoconiosis is usually caused by exposure to crystalline mineral fibres and particles. This dissertation explores which genes are activated or eliminated after lung cell exposure to asbestos or coal mine dust and which mechanisms play a role in the development of such diseases. The ‘inflammasome’ protein was found to play an important role in the inflammation underlying this disease. In addition, it was shown that activation of this protein in lung cells in turn triggers reactions associated with tissue stiffening, a feature of occupational asbestosis and silicosis. Furthermore, it was found that this protein can also play a role in the development of the disease in miners suffering from pneumoconiosis. This study may contribute to the development of new drugs.
Original language | English |
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Qualification | Doctor of Philosophy |
Awarding Institution |
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Supervisors/Advisors |
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Award date | 29 May 2015 |
Place of Publication | Maastricht |
Publisher | |
Print ISBNs | 9789461594426 |
DOIs | |
Publication status | Published - 2015 |
Keywords
- asbestosis
- silicosis
- pathogenic mechanisms