[Nicotinic receptor polymorphism amplifies cigarette smoke-induced inflammation in COPD, a silent epidemic].

Chronic obstructive pulmonary disease (COPD) is the third leading cause of mortality and morbidity. Recent studies on genetic polymorphism highlight the CHRNA5/3/B4 locus, coding for nicotinic subunit receptors such as rs16969968 polymorphism (α5SNP), as genetic determinants of pulmonary vulnerability, acting independently of smoking intensity. We have demonstrated that altered α5 nicotinic receptor expression influences epithelial differentiation, promotes inflammation, and drives airway remodeling. These findings point to a functional role of the pulmonary nicotinic system in COPD pathogenesis and underline the need for precision medicine approaches combining genetic, environmental, and clinical markers so as to better predict disease risk and develop relevant preventive strategies.