Current smoking contributes to a poorer asthma prognosis and more severe symptoms and limits corticosteroids’ therapeutic benefits. The nasal epithelium is a good place to look for changes in gene expression and DNA methylation since it can reflect smoking-induced alterations in the lower airways. The alterations in gene expression and DNA methylation in current and ex-smokers with asthma were investigated in this study. The researchers assessed matched gene expression and epigenome-wide DNA methylation samples taken from nasal brushings of 55 patients engaged in a clinical trial of current and ex-smoker asthma patients. Current smokers and ex-smokers were compared using differential gene expression and DNA methylation studies. Researchers did an expression quantitative trait methylation (eQTM) analysis to investigate smoking-relevant genes by CpG sites that differ between current and ex-smokers. Significant CpG sites were investigated in bronchial samples from people who had quit smoking to see if smoking-related DNA methylation modifications were relevant for the lower airways. A total of 809 genes and 18,814 CpG sites were significantly linked with current nasal smoking. AHRR, ALDH3A1, CYP1A1, and CYP1B1 were among the 171 CpG sites identified by the cis-eQTM analysis as having a methylation status linked with smoking-related gene expression.

After one year of smoking cessation, they restored the methylation status of CpG sites affected by current smoking. Current smoking modifies epigenetic patterns and gene expression in the nasal epithelium of asthma patients, which is partially reversible in bronchial biopsies after smoking cessation. Researchers demonstrated that molecular changes can be detected in the nasal epithelium, and they provide this as a tool for future research into the disease-related effects of cigarette smoke.