Study On The Relationship Between IL6R And IL-5RA Gene Polymorphisms And Chronic Obstructive Pulmonary Disease(COPD) In Hainan Han Population

Objective:Chronic obstructive pulmonary disease(COPD)is a kind of pulmonary inflammatory disease with high morbidity and mortality.Studies have found that interleulcin 6 receptor(IL6R)and Interleukin 5 Receptor Subunit Alpha(IL5RA)mutants have an impact on the pathogenesis of COPD.Therefore,the purpose of this study was to discuss the relationship between IL-6R and IL5RA mutation sites and the susceptibility to COPD and summarize the research progress of COPD.Methods:The study included 996 subjects,including 498 COPD patients and 498 healthy individuals.Multiple genetic models were used to analyze the relationship between IL6R polymorphism and COPD risk.The correlation strength between single nucleotide polymorphism(SNP)and COPD risk was evaluated by calculating odds ratio(ORs)and 95%confidence interval(95%CI).In addition,multi factor dimensionality reduction(MDR)is used to predict the interaction between SNPs.Results:In the overall analysis results,IL6R rs6689306(OR=2.08,p=7.782E16),IL6R rs4845625(OR=197,p=1.256E-13)and IL5RA rs3856850(OR=1.22,p=0.030)promoted the development of susceptibility to COPD,and IL6R rs4537545(OR=0.49,p=2.706E-13),IL6R rs4129267(OR=0.48,p=2.961E-14),IL6R rs2228145(OR=0.49,p=7.636E-14)and ILSRA rs13097407(OR=0.43,p=5.6E-05)significantly reduced the risk of COPD.In the stratified analysis,IL6R rs4537545,IL6R rs4129267,IL6R rs2228145 and IL5RA rs13097407 were related to the reduction of COPD risk in different subgroups.And MDR analysis pointed out that the interaction model built by IL6R SNP rs689306,rs4537545,rs4845625,rs4129267,rs2228145 and IL5RA SNP rs3804795,rs2290610,rs13097407,rs334782,rs3856850 is the best five-site model for predicting COPD(CVC=10/10,p<0.0001).Conclusion:The results showed that IL6R gene polymorphism was significantly associated with the susceptibility to COPD.This discovery expands the theoretical basis of the pathogenesis of COPD and provides a direction for further research on its molecular mechanism.