EPIGENETIC PROGRAMMING OF THE SINONASAL MUCOSA: IMPLICATIONS FOR ALLERGIC RHINITIS AND AIRWAY INFLAMMATION

Allergic rhinitis and allergic asthma are increasingly recognized as manifestations of a unified airway disease characterized by chronic epithelial inflammation, immune dysregulation, and allergic sensitization. Although genetic predisposition contributes to disease susceptibility, the rapid rise in allergic diseases cannot be explained solely by genetic factors. Epigenetic mechanisms, including DNA methylation, histone modifications, chromatin remodeling, and non-coding RNA regulation, have emerged as key mediators linking environmental exposures to immune dysfunction and allergic inflammation. This review examines current evidence regarding the role of epigenetic regulation in allergic sensitization, with particular focus on allergic rhinitis and allergic asthma. The effects of early-life environmental exposures, air pollution, tobacco smoke, microbial dysbiosis, and dietary factors on epigenetic programming are discussed. The review also explores the interactions between epithelial barrier dysfunction, microbiome alterations, and epigenetic regulation within the united airway system. Growing evidence suggests that many epigenetic alterations are potentially reversible, creating new opportunities for preventive and therapeutic interventions. Advances in nutriepigenetics, microbiome research, and precision medicine may facilitate the development of individualized strategies aimed at restoring immune tolerance and reducing chronic airway inflammation. Understanding the epigenetic mechanisms underlying allergic sensitization may therefore contribute to more effective prevention, risk stratification, and personalized management of allergic airway diseases. Keywords: allergic rhinitis, asthma, epigenetics, allergic sensitization, DNA methylation, microbiome, epithelial barrier, united airway disease, precision medicine, nutriepigenetics