Chronic rhinosinusitis (CRS) is a widespread inflammatory condition affecting the nasal and sinus cavities, impacting millions globally. Although the underlying mechanisms of CRS are not yet fully understood, recent research suggests a dynamic interplay between various immune and epithelial cells plays a key role in driving the disease.

Methodology

Single-cell sequencing and Spatial transcriptomics were employed in conjunction to analyze the phenotypic composition and functional aspects of a discovery CRS clinical cohort. The aim was to identify key players and epithelial-immune interactions within inflamed nasal tissues, including CRSwNP. This approach provides a valuable resource applicable to various nasal inflammatory diseases.

Results

The study uncovered several critical findings:

1.   Macrophage-Eosinophil Recruitment: Mechanisms for the recruitment of macrophages and eosinophils into the nasal mucosa were identified.
2.   T Cell Dysregulation: A systematic dysregulation of CD4+ and CD8+ T cells was observed in CRS.
3.   Mast Cell Enrichment: An enrichment of mast cell populations in the upper airway tissues, with intricate interactions between mast cells and CD4 T cells was observed.
4.   Immune-Epithelial Interactions: Significant immune-epithelial interactions and dysregulation, particularly involving basal progenitor cells and Tuft chemosensory cells were identified.
5.     Basal Cell Trajectory: A distinct basal cell differential trajectory was noted in CRS patients with nasal polyps, linked to polyp formation through immune-epithelial remodeling.

Implications

These findings enhance the understanding of nasal inflammation and provide a comprehensive resource for exploring the cellular and molecular mechanisms underlying CRS and other nasal inflammatory diseases. This knowledge paves the way for developing more precise and effective treatments, ultimately improving patient outcomes.