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The -463G/A and -129G/A myeloperoxidase-encoding gene polymorphism in chronic obstructive pulmonary disease
Andrzej Witusik1, Łukasz Mokros2, Janusz Szemraj3
1Grażyna and Kiejstut Bacewicz Memorial Academy of Music in Łódź, Faculty of Composition, Theory of Music, Conducting, Eurhythmics and Music Education, Music Therapy Course, Łódź, Poland.
Introduction:
Neutrophils are involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). Myeloperoxidase is an important bactericidal granulocytic enzyme. It is of interest to question whether or not the polymorphic variants of the myeloperoxidase-encoding gene are associated with the risk of developing COPD.
Material And Methods:
The study determined the risk of COPD development in 186 COPD patients and 220 healthy subjects in the context of two selected polymorphic sites of the promoter region of the myeloperoxidase-encoding gene.
Results:
It has been demonstrated that the AA genotype of locus -463 in the myeloperoxidase-encoding gene increases the risk of developing COPD (OR: 2.87; CI: 1.651-4.997). This genotype also correlates with a higher gene expression in patients (0.56 ± 0.12 vs 0.31 ± 0.18 in patients with AG genotype and 0.29 ± 0.17, p < 0.01 in those with GG genotype). In healthy indivi-duals, the AA genotype was also characterized by increased expression of the myeloperoxidase-encoding gene (0.41 ± 0.16 vs 0.29 ± 0.15 for AG genotype, p < 0.01 and 0.25 ± 0.16 for GG genotype p < 0.01). Patients with the AA genotype had a significantly higher gene expression than healthy subjects with this genotype.
Conclusions:
The polymorphic site -129 of the myeloperoxidase-encoding gene was unrelated to the development of COPD. The gene expression did not differ for the individual genotypes. Our studies indicate that the polymorphism of the myeloperoxidase--encoding gene may be related to chronic obstructive pulmonary disease.
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