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MMP-1(-1607G) polymorphism as a risk factor for fibrosis after pulmonary tuberculosis in Taiwan

C-H Wang1, H-C Lin, S-M Lin

  • 1Department of Thoracic Medicine, Chang Gung Memorial Hospital, Taipei, Taiwan.

The International Journal of Tuberculosis and Lung Disease : the Official Journal of the International Union Against Tuberculosis and Lung Disease
|April 16, 2010
PubMed
Abstract

Insights

Matrix metalloproteinase-1 (MMP-1) gene variations increase the risk of severe lung fibrosis after tuberculosis treatment. This finding may guide personalized risk assessment for pulmonary tuberculosis patients.

Area of Science:

  • Genetics and Molecular Biology
  • Pulmonology
  • Infectious Diseases

Background:

  • Matrix metalloproteinase (MMP) gene polymorphisms are implicated in lung fibrosis development post-pulmonary tuberculosis (TB).
  • Understanding these genetic associations is crucial for predicting TB-related lung damage.

Purpose of the Study:

  • To investigate the association between MMP-1, MMP-9, and MMP-12 polymorphisms and the development of lung fibrosis in pulmonary TB patients.

Main Methods:

  • A study involving 49 healthy subjects and 98 TB patients.
  • Analysis of MMP-1, MMP-9, and MMP-12 polymorphisms and their correlation with lung fibrosis indices via serial chest radiography over one year post-treatment.

Main Results:

  • The MMP-1(-1607G) polymorphism was significantly more frequent in TB patients with moderate to advanced lung fibrosis.
  • Individuals with at least one -1607G MMP-1 allele had a 5-fold increased risk of moderate and a 9.87-fold increased risk of advanced fibrosis.
  • No significant association was found for MMP-9(-1562T) or MMP-12(Asn357Ser) polymorphisms with lung fibrosis. Increased MMP-1 production was observed in subjects with the 1G allele.

Conclusions:

  • The MMP-1(-1607G) polymorphism is linked to increased vulnerability to extensive lung fibrosis one year after tuberculosis treatment.
  • This heightened risk may stem from elevated MMP-1 activity, promoting matrix degradation and subsequent fibrotic changes.

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