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Updated: Aug 20, 2025

Use of the EpiAirway Model for Characterizing Long-term Host-pathogen Interactions
Published on: September 2, 2011
Unified Airway Disease: Genetics and Epigenetics
Tripti Brar1, Michael J Marino1, Devyani Lal1
1Department of Otolaryngology- Head & Neck Surgery, Division of Rhinology, Mayo Clinic in Arizona, 5777 East Mayo Boulevard, Phoenix, AZ 85054, USA.
Abstract:
Although unified airway disease (UAD) may have heritable components, genetic changes involving coexistent chronic rhinosinusitis (CRS) are not well understood. Genetic predisposition is stronger in patients with CRS with nasal polyps compared with those without nasal polyps (CRSsNP). Genetic factors account for 25% to 80% of asthma risk and 90% of allergic rhinitis risk but risk contributions are not well described for CRS. Susceptibility genes identified in coexistent CRS-asthma relate to innate and adaptive immunity, cytokine signaling, tissue remodeling, arachidonic acid metabolism, and other proinflammatory pathways. Non-type 2 UAD such as CRS-bronchitis/bronchiectasis and CRSsNP are currently inadequately characterized.
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