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

CH Wang, HC Lin, SM Lin, CD Huang… - … of Tuberculosis and …, 2010 - ingentaconnect.com
CH Wang, HC Lin, SM Lin, CD Huang, CY Liu, KH Huang, LL Hsieh, KF Chung, HP Kuo
The International Journal of Tuberculosis and Lung Disease, 2010ingentaconnect.com
SETTING: Several matrix metalloproteinase (MMP) polymorphisms favouring the
development of lung fibrosis after pulmonary tuberculosis (TB) have been described.
OBJECTIVE: To investigate the association of MMP-1, MMP-9 and MMP-12 polymorphisms
with the development of fibrosis in pulmonary TB. DESIGN: We studied 49 normal subjects
and 98 TB patients. We analysed the association between MMP polymorphisms and clinical
indices of lung fibrosis by serial chest radiography for 1 year after completion of treatment …
SETTING
Several matrix metalloproteinase (MMP) polymorphisms favouring the development of lung fibrosis after pulmonary tuberculosis (TB) have been described.
OBJECTIVE
To investigate the association of MMP-1, MMP-9 and MMP-12 polymorphisms with the development of fibrosis in pulmonary TB.
DESIGN
We studied 49 normal subjects and 98 TB patients. We analysed the association between MMP polymorphisms and clinical indices of lung fibrosis by serial chest radiography for 1 year after completion of treatment.
RESULTS
The frequency of the MMP-1(-1607G) polymorphism was significantly higher in TB patients with moderate to advanced pulmonary fibrosis than in those with minimal to mild fibrosis. Having at least one -1607G MMP-1 polymorphism increased the risk of moderate and advanced fibrosis respectively by 5.04 (95%CI 1.25–20.30) and 9.87 (95%CI 2.39–40.88) fold. There was no association of MMP-9(-1562T) and MMP-12(Asn357Ser) polymorphisms with lung fibrosis. The production of MMP-1 from monocytes stimulated by interleukin-1β was increased in subjects with the 1G allele genotype compared to the 2G/2G genotype.
CONCLUSIONS
Patients with MMP-1(-1607G) polymorphism are more vulnerable to more extensive lung fibrosis 1 year after anti-tuberculosis treatment. This may be related to increased MMP-1 activity, leading to enhanced destruction of the matrix with subsequent fibrosis.
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