Nasal Cytology as a Cellular Window into Epithelial Dysfunction and Type 2 Inflammation: From Mechanisms to Translational Implications.

Epithelial barrier dysfunction is increasingly recognized as a central pathogenic mechanism in chronic inflammatory airway diseases characterized by type 2 immune responses. Chronic rhinosinusitis with nasal polyps (CRSwNP) represents a paradigmatic condition in which structural epithelial alterations, impaired barrier integrity, and sustained release of epithelial-derived alarmins interact with innate and adaptive immune pathways to drive persistent inflammation and tissue remodeling. In this context, understanding disease heterogeneity requires tools capable of capturing cellular and immunological complexity beyond purely molecular or symptom-based classifications. Nasal cytology is a standardized, minimally invasive, and repeatable technique that provides direct in vivo assessment of epithelial morphology and inflammatory cell infiltrates at the mucosal surface. By identifying distinct cytological patterns, including eosinophil-dominant, mast cell-rich, and mixed inflammatory signatures, nasal cytology reflects the underlying immunopathological mechanisms of CRSwNP and correlates with disease severity, clinical control, and therapeutic responsiveness. Its dynamic nature allows longitudinal monitoring of inflammatory changes over time, offering insights that complement clinical evaluation and endoscopic assessment. This review integrates current knowledge on epithelial barrier dysfunction and type 2 inflammation with the translational relevance of nasal cytology in CRSwNP. Particular attention is given to its role in disease phenotyping, prognostic stratification, and monitoring of biologic therapies. Within precision medicine frameworks, nasal cytology emerges as a robust cellular biomarker bridging epithelial biology, immune profiling, and personalized clinical decision-making.