TY - JOUR T1 - Association of HTR2A-1438G/A Genetic Polymorphism With Smoking and Chronic Obstructive Pulmonary Disease JO - Archivos de Bronconeumología T2 - AU - Verde,Zoraida AU - Santiago,Catalina AU - Chicharro,Luis M. AU - Bandrés,Fernando AU - Gómez-Gallego,Félix AU - Rodríguez González-Moro,Jose Miguel AU - de Lucas,Pilar SN - 03002896 M3 - 10.1016/j.arbres.2018.07.021 DO - 10.1016/j.arbres.2018.07.021 UR - https://archbronconeumol.org/en-association-htr2a-1438g-a-genetic-polymorphism-with-articulo-S0300289618303144 AB - IntroductionCigarette smoking is a major risk factor in the development of chronic obstructive pulmonary disease (COPD). Serotonin levels have been associated with COPD and smoking has been as a significant modulator. Elevated levels of serotonin are responsible for bronchoconstriction and pulmonary vasoconstriction and also nicotine dependence, thus serotonin response could be affected by genetic polymorphisms in transporters and receptors of serotonin. ObjectivesThe aim of the current study was to analyze the effect of SLC6A4 (5HTT_LPR) (rs25531) and HTR2A-1438G/A (rs6311) genetic polymorphisms on the relation between smoking habits and COPD. MethodsThe association between SLC6A4 (5HTT_LPR) (rs25531), HTR2A-1438G/A (rs6311), smoking degree and COPD was analyzed in a total of 77 COPD patients (active smokers) and 90 control subjects (active healthy smokers). The DNA was extracted of peripheral leukocytes samples and genotyping was performed using an allele specific polymerase chain reaction. ResultsThe distribution of SLC6A4 genotypes did not vary between healthy smokers and COPD patients (P=0.758). On the other hand, the A allele of HTR2A (rs6311) was significantly associated with COPD incidence in the trend model (P=0.02; 1.80 [1.04–3.11]). Among all smokers, this allele was also associated with the number of pack years smoked (P=0.02) and also, we observed a marginal association with FEV1/FVC values (P=0.06). ConclusionOur results point a possible role of the A allele of HTR2A (rs6311) in COPD pathogenesis, suggesting that this effect depends partly on tobacco consumption due to a gene-by-environment interaction. ER -