Identification of differentially methylated sites in COPD by exposure to biomass smoke

Chronic obstructive pulmonary disease (COPD) is a complex and multifactorial pathology. It is characterized by persistent respiratory symptoms and is due, among other causes, to airway and/or alveolar abnormalities, generally caused by exposure to particulate matter or noxious gases. Biomass smoke exposure is an environmental risk factor that can modify methylation patterns in genes that participate or contribute to the development of COPD. The best known epigenetic mechanism in humans is cytosine methylation, which occurs by covalent modification of carbon 5 of cytosine (5-methyl cytosine, 5mC), mostly present in CG dinucleotides within the genome. CG dinucleotides tend to be in sequences called cytosine CpGon 5 (5-methyl cytosine, 5mC) islands, they are mostly present in CG dinucleotides within the genome. CG dinucleotides tend to be in sequences called CpG islands. An epigenome-wide association study was performed using the Illumina EPIC Infinium Methylation microarray in induced sputum samples from 45 women with COPD from biomass smoke exposure (EP-HL) and 46 women without COPD but with biomass smoke exposure (EXP-HL). The bioinformatic and statistical analysis was performed in the Rstudio environment.