Tumor necrosis factor-α gene promoter polymorphism is not associated with smoking-related COPD in Thailand

被引:31
作者
Chierakul, N [1 ]
Wongwisutikul, P
Vejbaesya, S
Chotvilaiwan, K
机构
[1] Mahidol Univ, Siriaj Hosp, Fac Med, Dept Med,Div Resp Dis & TB, Bangkok 10700, Thailand
[2] Mahidol Univ, Siriaj Hosp, Fac Med, Dept Transfus Med, Bangkok 10700, Thailand
关键词
chronic obstructive pulmonary disease; genetics; polymorphism; susceptibility; tumour necrosis factor-alpha;
D O I
10.1111/j.1440-1843.2005.00626.x
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
Objective: Susceptibility to COPD is, in part, genetically determined. Tumour necrosis factor (TNF)-alpha gene promoter polymorphisms have been investigated in different populations with inconsistent results. This study aimed to determine the genetic predisposition in Thai smoking-related COPD patients. Methodology: The polymorphism at position -308 of the TNF-alpha gene promoter was examined in 57 patients with smoking-related COPD, 67 smoker control subjects, and 116 control anonymous blood donors. Genomic DNA from peripheral blood lymphocytes was used for genotypic analysis by polymerase chain reaction with sequence specific primers. Results: TNF-alpha-308*2 allele frequency was not significantly different between the population control subjects and the smoking-related COPD patients (4.7% vs. 7.9%, P = 0. 14). This allele frequency was also not significantly different between smokers with and without COPD (7.9% vs. 7.5%, P 0.46). Conclusions: Although it has been speculated that TNF-alpha might have a causal relationship with COPD, a role for the TNF-alpha gene promoter polymorphism in disease development in Thailand was not demonstrated.
引用
收藏
页码:36 / 39
页数:4
相关论文
共 20 条
[1]   Activation of the TNF alpha-p55 receptor induces myocyte proliferation and modulates agonist-evoked calcium transients in cultured human tracheal smooth muscle cells [J].
Amrani, Y ;
Panettieri, RA ;
Frossard, N ;
Bronner, C .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1996, 15 (01) :55-63
[2]   Tumor necrosis factor-α is central to acute cigarette smoke-induced inflammation and connective tissue breakdown [J].
Churg, A ;
Dai, J ;
Tai, H ;
Xie, CS ;
Wright, JL .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2002, 166 (06) :849-854
[3]  
*DEP EP MIN PUBL H, 1991, 1 NAT HLTH SURV THAI
[4]   TNF-alpha inhibits isoproterenol-stimulated adenylyl cyclase activity in cultured airway smooth muscle cells [J].
Emala, CW ;
Kuhl, J ;
Hungerford, CL ;
Hirshman, CA .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 1997, 272 (04) :L644-L650
[5]   Polymerase chain reaction haplotyping using 3' mismatches in the forward and reverse primers: Application to the biallelic polymorphisms of tumor necrosis factor and lymphotoxin alpha [J].
Fanning, GC ;
Bunce, M ;
Black, CM ;
Welsh, KI .
TISSUE ANTIGENS, 1997, 50 (01) :23-31
[6]   Tumour necrosis factor family genes in a phenotype of COPD associated with emphysema [J].
Ferrarotti, I ;
Zorzetto, M ;
Beccaria, M ;
Gilè, LS ;
Porta, R ;
Ambrosino, N ;
Pignatti, PF ;
Cerveri, I ;
Pozzi, E ;
Luisetti, M .
EUROPEAN RESPIRATORY JOURNAL, 2003, 21 (03) :444-449
[7]   Influence of TNFα gene polymorphisms on TNFα production and disease [J].
Hajeer, AH ;
Hutchinson, IV .
HUMAN IMMUNOLOGY, 2001, 62 (11) :1191-1199
[8]   Tumour necrosis factor-α gene promoter polymorphism in chronic obstructive pulmonary disease [J].
Higham, MA ;
Pride, NB ;
Alikhan, A ;
Morrell, NW .
EUROPEAN RESPIRATORY JOURNAL, 2000, 15 (02) :281-284
[9]   Tumor necrosis factor-alpha gene polymorphism in chronic bronchitis [J].
Huang, SL ;
Su, CH ;
Chang, SC .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1997, 156 (05) :1436-1439
[10]   Neither IL-1β, IL-1 receptor antagonist, nor TNF-α polymorphisms are associated with susceptibility to COPD [J].
Ishii, T ;
Matsuse, T ;
Teramoto, S ;
Matsui, H ;
Miyao, M ;
Hosoi, T ;
Takahashi, H ;
Fukuchi, Y ;
Ouchi, Y .
RESPIRATORY MEDICINE, 2000, 94 (09) :847-851