Lack of the Association between Microsatellite Polymorphism in Toll-like Receptor 2 Gene and Development of COPD.
10.4046/trd.2005.58.4.367
- Author:
Hee Seok LEE
1
;
Hye Won LEE
;
Deog Kyeom KIM
;
Dong Seok KO
;
Gun Min PARK
;
Yong Il HWANG
;
Sang Min LEE
;
Chul Gyu YOO
;
Young Whan KIM
;
Sung Koo HAN
;
Young Soo SHIM
;
Jae Joon YIM
Author Information
1. Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine and Lung Institute of Medical Research Center, Seoul National University College of Medicine, Korea. yimjj@snu.ac.kr
- Publication Type:Original Article
- Keywords:
Chronic obstructive pulmonary disease (COPD);
Toll-like receptor 2 (TLR2);
Microsatellite polymorphism;
Genetic susceptibility
- MeSH:
Alleles;
Blood Donors;
Dinucleotide Repeats;
Extracellular Matrix;
Genetic Predisposition to Disease;
Genotype;
Humans;
Introns;
Lung;
Male;
Microsatellite Repeats*;
Pulmonary Disease, Chronic Obstructive*;
Pulmonary Surfactant-Associated Protein A;
Tobacco Products;
Toll-Like Receptor 2*;
Toll-Like Receptors*
- From:Tuberculosis and Respiratory Diseases
2005;58(4):367-374
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: The fact that only 10-20% of chronic cigarette smokers develop chronic obstructive pulmonary disease (COPD) reflects the presence of genetic factors associated with the susceptibility to COPD. Recently, it was reported that the surfactant protein A increases the secretion of matrix metalloprotease 9, which degrades extracellular matrices of the lung, through a Toll-like receptor 2 (TLR2). In this context, possible role of TLR2 in the pathogenesis of COPD was postulated, and a functional dinucleotide repeat polymorphism in intron II of TLR2 was evaluated for any association with COPD. METHOD: Male patients with COPD and male smokers with a normal pulmonary function were enrolled in this study. The number of Guanine-Thymine repeats in intron II of the TLR2 gene were counted. Because the distributions of the repeats were trimodal, the alleles were classified into three subclasses, 12-16 repeats: short (S) alleles; 17-22 repeats: medium length (M) alleles; and 23-27 repeats: long (L) alleles. RESULT: 125 male patients with COPD and 144 age- and gender-matched blood donors with a normal lung function were enrolled. There were no differences in the distribution of each allele subclass (S, M and L) between the COPD and control group (p=0.75). The frequencies of the genotypes with and without each allele subclass in the COPD and control group were similar. CONCLUSION: A microsatellite polymorphism in intron II of TLR2 gene was not associated with the development of COPD in Koreans.
