Impact of GSTM1, GSTT1, and IL-4 R(α) genetic polymorphisms toward susceptibility for Chronic Obstructive Pulmonary Disease (COPD)

Abstract

The progressive inflammatory lung disease known as chronic obstructive pulmonary disorder (COPD) is characterised by persistent respiratory symptoms and restricted airflow. Due to the intricate interactions between genetic and environmental factors, the pathophysiology of COPD is complex and heterogeneous. Numerous studies have looked into the relationship between the polymorphisms in the genes GSTM1, GSTT1, and IL-4R(α) and the risk of COPD in different ethnic groups and subgroups. However, the information we have so far is inconsistent. We conducted the study to look into the potential impact of the polymorphisms in GSTM1, GSTT1, and IL-4R(α) on the likelihood of developing COPD, either individually or in combination. For GSTM1 and GSTT1 polymorphisms, a total of 400 subjects (200 cases and 200 controls) were examined, and a total of 405 subjects (202 cases and 203 controls) were examined for IL-4R(α) polymorphism. Multiplex PCR was used to genotype the GSTM1 and GSTT1 genes, and PCR-RFLP was used to genotype the IL-4R(α) gene. Compared to controls, COPD cases (34.5%) had a higher rate of GSTT1 gene deletion (20.5%). The GSTT1(-) null genotype was found to have a significant statistical association with COPD risk (OR = 2.04, p = 0.0019, 95 percent CI = 1.30-3.20). A strong correlation between the null genotype of GSTT1(-) and COPD risk was discovered after adjusting for covariates like age, gender, and smoking status (AOR =2.90, p=0.003, 95 percent CI=1.43- 5.87). Additionally, a significant relationship between clinical parameters for COPD risk and GSTT1(-) genotype was observed. Another major observation was that females with GSTT1(- ) null genotype were more vulnerable to COPD than males with the same gene deletion. However, no such significant association was observed in GSTM1 and IL-4R(α) polymorphisms towards the COPD susceptibility. In conclusion, GSTT1 polymorphism might play a vital role as biomarker for clinical prediction in COPD.