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

**Authors:** Matteo Gelardi

PMC · DOI: 10.3390/cells15040323 · 2026-02-10

## TL;DR

Nasal cytology offers a minimally invasive way to study epithelial dysfunction and inflammation in chronic airway diseases like nasal polyps.

## Contribution

The paper highlights nasal cytology as a novel translational tool for understanding and managing type 2 inflammation in chronic rhinosinusitis.

## Key findings

- Nasal cytology reveals distinct inflammatory patterns linked to CRSwNP immunopathology.
- Cytological profiles correlate with disease severity and response to treatment.
- The technique supports personalized medicine by bridging epithelial biology and immune profiling.

## Abstract

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.

## Full-text entities

- **Genes:** IL13 (interleukin 13) [NCBI Gene 3596] {aka IL-13, P600}, IL5 (interleukin 5) [NCBI Gene 3567] {aka EDF, IL-5, TRF}, TSLP (thymic stromal lymphopoietin) [NCBI Gene 85480], IL4 (interleukin 4) [NCBI Gene 3565] {aka BCGF-1, BCGF1, BSF-1, BSF1, IL-4}, OCLN (occludin) [NCBI Gene 100506658] {aka BLCPMG, PPP1R115, PTORCH1}, IGHE (immunoglobulin heavy constant epsilon) [NCBI Gene 3497] {aka IgE}, IL25 (interleukin 25) [NCBI Gene 64806] {aka IL17E}, IL33 (interleukin 33) [NCBI Gene 90865] {aka C9orf26, DVS27, IL1F11, NF-HEV, NFEHEV}
- **Diseases:** epithelial (MESH:D009375), eosinophilic disease (MESH:D017681), nasal polyposis (MESH:D009668), infective (MESH:D007239), antrochoanal polyps (MESH:D011127), Chronic rhinosinusitis (MESH:D000092562), chronic (MESH:D002908), fibrosis (MESH:D005355), 2 inflammation (MESH:D007249), injury to (MESH:D014947), eosinophilia (MESH:D004802), airway diseases (MESH:D029424), CRSwNP (MESH:D009298)
- **Chemicals:** Hematoxylin (MESH:D006416), mepolizumab (MESH:C434107), lipid (MESH:D008055), dupilumab (MESH:C582203), eosin (MESH:D004801), omalizumab (MESH:D000069444)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12939964/full.md

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Source: https://tomesphere.com/paper/PMC12939964