Effect of a disintegrin and metalloprotease 33 (ADAM33) gene polymorphisms and smoking in COPD

Abstract

Background: COPD is characterized by air flow limitation that is not fully reversed and associated with an influx of neutrophils, macrophages and CD8 T lymphocytes in the airways. The disease is characterized by airflow limitation and is associated with an abnormal inflammatory response of the lungs in response to noxious particles or gases and associated with systemic manifestation. Methods: Sixty consecutive patients with COPD and 40 normal healthy individuals were included. All cases and controls were subjected to detection of 2 polymorphic loci (S1 AND Q1) of ADAM33 by PCR-RFLP technique. Results: The percentage of S1 and Q1 AA genotype and A allele were significantly increased in control than in COPD patients while there was significant increase in S1 and Q1 GG genotype and G allele in COPD patients than in control (p 0.05, whereas there was significant increase in ADAM33 S1 G allele and Q1 G allele in smoker and non-smoker in COPD patients as compared to their corresponding fellows in control group (p < 0.05). As regard to Pulmonary function test there was significant decrease in % of FEV1 in COPD patients as compared to control group for both smokers and non-smokers (p < 0.001). Within both control and COPD groups smokers had significant decrease in FEV1 % as compared to non-smokers (p < 0.001). There was a significant decrease in FEV1 % among all genotypes in smoker as compared to non-smoker COPD patients (p < 0.001), the most prominent decrease was found in smoker GG genotype for both ADAM33 S1 and Q1 in COPD patients. Conclusion: In conclusion, we found that polymorphisms in the SNPs (Q1 and S1) of ADAM33 gene are associated with COPD in the general population. In addition, smoker patients with GG genotype in (S1 and Q1) ADAM33 will have more pronounced decline in the pulmonary function test (FEV1).

Keywords

• COPD
• Disintegrin
• Metalloprotease
• Gene polymorphisms