Association of TNF-α–308G/A, SP-B 1580 C/T, IL-13 –1055 C/T gene polymorphisms and latent adenoviral infection with chronic obstructive pulmonary disease in an Egyptian population

Abstract

IntroductionChronic obstructive pulmonary disease (COPD) is a leading cause of disability and death. The most common cause of COPD is smoking. There is evidence suggesting that genetic factors influence COPD susceptibility and variants in several candidate genes have been significantly associated with COPD. In this study, we aimed to investigate the possible association of the TNF-α –308, SPB+1580, IL-13 –1055 gene polymorphisms and latent adenovirus C infection with COPD in an Egyptian population.Material and methodsOur study included 115 subjects (75 smokers with COPD, 25 resistant smokers and 15 non-smokers) who were subjected to spirometric measurements, identification of adenovirus C and genotyping of TNF-α –308G/A, SP-B+1580 C/T and IL-13 –1055 C/T polymorphisms by real-time PCR.ResultsThe adenovirus C gene was identified in all subjects. The distribution of TNF-α genotypes showed no significant differences between different groups. However, homozygous A genotype was associated with a significant decrease in FEV1, FEV1/FVC and FEF25/75% of predicted in COPD (p < 0.05). As regards SP-B genotypes, resistant smokers had a significantly higher homozygous T genotype frequency compared to COPD and non smokers (p = 0.005). Interleukin 13 genotypes showed no significant difference between different groups. There was a significant decrease in FEF25/75% of predicted in T allele carriers in COPD patients (p = 0.001).ConclusionsThe COPD is a disease caused by the interaction of combined genes and environmental influences, in the presence of smoking and latent adenovirus C infection, TNF-α –308A, SPB +1580 T and IL-13 –1055 T polymorphisms predispose to the development of COPD.

Systematic review/Meta-analysis Interleukin-1B-31T/C promoter polymorphism and chronic obstructive pulmonary disease risk: a meta-analysis

“…To date, although the underlying mechanisms of COPD remain not fully elucidated, a genetic predisposition of COPD has been strongly evidenced [2–4]. …”

Association of the CYP1A1 MspI and TNFα-308 polymorphisms with chronic obstructive pulmonary disease in Inner Mongolia

“…Studies in Taiwanese (Huang et al, 1997), Japanese (Sakao et al, 2001), and Caucasian smokers (Gingo et al, 2008) showed similar results to those of the present study in demonstrating that the TNFα-308 polymorphism is a risk factor of COPD. However, studies in Thai (Chierakul et al, 2005), adenovirus C-infected Egyptian (Ezzeldin et al, 2012), Caucasian (Higham et al, 2000;Chappell et al, 2007), German (Seifart et al, 2005), and European-descended American (Tanaka et al, 2007) subjects showed opposite results. Teramoto et al (2008) stated that the TNFα-308 polymorphism was not associated with susceptibility to Asian COPD.…”

Impact of respiratory viruses on the course of chronic obstructive pulmonary disease: Towards optimizing treatment

“…Это свидетельствует, что хроническая ВИ может поддер-живать воспаление в дыхательных путях и увеличивать тяжесть ХОБЛ стабильного течения. В поддержку этого тезиса можно привести данные о роли латентной аденовирусной инфекции, которая у лиц с генетической предрасположенностью способ-ствует развитию и прогрессированию ХОБЛ у курящих людей [24].…”