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Article

Interleukin gene polymorphisms in pneumoconiosis

  • Authors:
    • Simone Helmig
    • Martin Grossmann
    • Jelena Wübbeling
    • Joachim Schneider
  • View Affiliations / Copyright

    Affiliations: Institute and Polyclinic for Occupational and Social Medicine, Justus-Liebig University, D-35392 Giessen, Germany
  • Pages: 401-408
    |
    Published online on: May 10, 2012
       https://doi.org/10.3892/ijmm.2012.996
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Abstract

Inhaled asbestos fibres are known to cause inflammation processes with the result of lung or pleural fibrosis and malignancies. Interleukins (IL), such as IL-1β, IL-6 and IL-10, have various functions in the regulation of the inflammatory response and in proliferative processes after inhalation of silica dust and can, therefore, influence the pathogenesis of asbestos-induced fibrosis and carcinogenesis. Polymorphisms within these genes may be associated with susceptibility to silica and asbestos-induced lung diseases. Thus, IL-1β, IL-6 and IL-10 polymorphisms were examined to determine an association with asbestos or silica-induced fibrosis or malignancies. Association studies were performed in 1180 individuals, using control subjects (n=177), fibrosis patients (n=605), lung cancer (LC) patients (n=364) and malignant mesothelioma (MM) patients (n=34). IL-1β (C-511T; C+3954T), IL-6 (G-174C) as well as IL-10 (G-1082A) polymorphisms were investigated. Compared to a healthy (control) group, a higher risk was seen for malignant mesothelioma patients in all investigated polymorphisms. The IL-6 -174C allele showed a tendency towards a higher risk for fibrosis or asbestos-induced lung cancer (ORasbestosis, 1.338; 95% CI, 0.71-2.53; ORsilicosis, 1.226; 95% CI, 0.54-2.81; ORfibrosis other aetiology, 1.313; 95% CI, 0.58-2.98 and ORLC asbestos, 2.112; 95% CI, 0.75-5.92). The IL-10 -1082A carrier seemed to be at higher risk for silicosis (ORsilicosis, 2.064; 95% CI, 0.78-5.49) but not for asbestosis. In summary, this study did not reveal sufficient evidence for a significant association of the investigated interleukin polymorphisms with asbestos or silica-induced diseases in the population studied.
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Copy and paste a formatted citation
Spandidos Publications style
Helmig S, Grossmann M, Wübbeling J and Schneider J: Interleukin gene polymorphisms in pneumoconiosis. Int J Mol Med 30: 401-408, 2012.
APA
Helmig, S., Grossmann, M., Wübbeling, J., & Schneider, J. (2012). Interleukin gene polymorphisms in pneumoconiosis. International Journal of Molecular Medicine, 30, 401-408. https://doi.org/10.3892/ijmm.2012.996
MLA
Helmig, S., Grossmann, M., Wübbeling, J., Schneider, J."Interleukin gene polymorphisms in pneumoconiosis". International Journal of Molecular Medicine 30.2 (2012): 401-408.
Chicago
Helmig, S., Grossmann, M., Wübbeling, J., Schneider, J."Interleukin gene polymorphisms in pneumoconiosis". International Journal of Molecular Medicine 30, no. 2 (2012): 401-408. https://doi.org/10.3892/ijmm.2012.996
Copy and paste a formatted citation
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Spandidos Publications style
Helmig S, Grossmann M, Wübbeling J and Schneider J: Interleukin gene polymorphisms in pneumoconiosis. Int J Mol Med 30: 401-408, 2012.
APA
Helmig, S., Grossmann, M., Wübbeling, J., & Schneider, J. (2012). Interleukin gene polymorphisms in pneumoconiosis. International Journal of Molecular Medicine, 30, 401-408. https://doi.org/10.3892/ijmm.2012.996
MLA
Helmig, S., Grossmann, M., Wübbeling, J., Schneider, J."Interleukin gene polymorphisms in pneumoconiosis". International Journal of Molecular Medicine 30.2 (2012): 401-408.
Chicago
Helmig, S., Grossmann, M., Wübbeling, J., Schneider, J."Interleukin gene polymorphisms in pneumoconiosis". International Journal of Molecular Medicine 30, no. 2 (2012): 401-408. https://doi.org/10.3892/ijmm.2012.996
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