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Tumour necrosis factor gene polymorphisms are associated with COPD

¹ Dept of Medicine, University of Colorado at Denver and Health Sciences Center, ² Dept of Medicine, National Jewish Medical and Research Center, and ³ Dept of Medicine, Denver Veterans Affairs Medical Center, Denver, CO, USA.

CORRESPONDENCE: R. P. Bowler, Division of Pulmonary Medicine, Dept of Medicine, National Jewish Medical and Research Center, 1400 Jackson Street, Room K715a, Denver, CO 80206, USA. Fax: 1 3032702249. E-mail: BowlerR{at}njc.org

Keywords: Gene polymorphism, genetics, smoking

Received: August 3, 2007
Accepted January 23, 2008

Tumour necrosis factor (TNF)- has been shown to be an important factor in animal models of chronic obstructive pulmonary disease (COPD). However, human studies of TNF polymorphisms in COPD have been equivocal.

Six TNF single nucleotide polymorphisms (-1031C/T, -863C/A, -857C/T, -237G/A, -308G/A and +487G/A) and their haplotypes were investigated in 423 Caucasian smokers (298 patients with spirometric evidence of COPD and 125 without airflow obstruction).

The -308 minor allele (A) had a higher odds ratio (OR) of being associated with COPD in multivariate analysis (controlling for age, sex, pack-yrs; OR 1.9, 95% confidence interval (CI) 1.1–3.2) and was also associated with worse forced expiratory volume in one second/forced vital capacity. The -237 minor allele (A) had a lower OR of being associated with COPD (OR 0.40, 95% CI 0.19–0.86). In COPD patients, the -857 minor allele (T) had a lower OR of being associated with severe stages of COPD (Global Initiative for Obstructive Lung Disease stage III and IV versus stage I and II, OR 0.46, 95% CI 0.24–0.88). Other TNF single nucleotide polymorphisms were not associated with COPD but the -1031/-863 haplotype CC/TC had a lower OR in COPD patients versus smoking controls (OR 0.22, 95% CI 0.05–0.97).

The present study adds further evidence that tumour necrosis factor genotypes play a role in susceptibility to cigarette smoke.

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