Chronic Inflammatory Pathways in Nasal Epithelial Disorders

Chronic inflammatory disorders of the nasal epithelium encompass conditions such as chronic rhinosinusitis with nasal polyps and allergic rhinitis, in which persistent type 2 immune responses, eosinophil infiltration and epithelial barrier dysfunction are central features. Nasal epithelial cells contribute to pathogenesis through secretion of cytokines, chemokines and antimicrobial peptides, while dysregulated signalling axes—including the high-affinity IgE receptor pathway and the balance between proteases and their inhibitors—drive both initiation and maintenance of inflammation. Transcriptomic profiling has revealed distinct gene and noncoding RNA signatures that differentiate eosinophilic from non-eosinophilic phenotypes, informing the pursuit of personalised biomarkers and targeted therapies. Environmental insults such as allergens, microbes and pollutants further disrupt epithelial junctions and amplify immune activation. Elucidating these interconnected molecular networks is crucial for developing strategies to prevent and treat chronic nasal inflammation and its systemic comorbidities.

Research from Nature Portfolio

Comprehensive RNA sequencing of nasal polyp tissue has revealed marked differences between eosinophilic and non-eosinophilic chronic rhinosinusitis with nasal polyps. This analysis identified novel long noncoding RNAs alongside key mRNAs that govern chemokine expression, immune-response pathways and extracellular matrix remodelling, providing a foundation for phenotype-specific diagnostics and therapeutic targets. In parallel, network analysis of matched nasal and bronchial epithelial brushings demonstrated a conserved pro-inflammatory gene module across the airway, notably involving cytochrome P450-mediated detoxification and innate immune signalling, while also highlighting regional divergence in cilia-associated pathways. Together, these studies underscore both the shared and unique aspects of epithelial inflammation throughout the respiratory tract, guiding the development of more precise interventions for chronic nasal disorders.

Chronic Inflammatory Pathways in Nasal Epithelial Disorders publication trend

The graph below shows the total number of articles in chronic inflammatory pathways in nasal epithelial disorders across all publications each year (not limited to Nature Index journals).

Technical terms

Type 2 (Th2) inflammation: An immune response driven by T-helper 2 cells producing interleukins IL-4, IL-5 and IL-13, promoting eosinophil recruitment and allergic-type reactions.

Eosinophils: Granulocytic white blood cells that release cytotoxic proteins and lipid mediators, central to allergic inflammation in the nasal mucosa.

Long noncoding RNA (lncRNA): Non-protein-coding transcripts longer than 200 nucleotides that regulate gene expression at multiple levels.

Transcriptomics: The large-scale study of RNA transcripts to profile gene expression patterns and identify disease-associated signatures.

Protease–antiprotease balance: The equilibrium between protein-degrading enzymes and their endogenous inhibitors, critical for maintaining epithelial barrier integrity.

FcεRI signalling pathway: A cascade initiated by IgE binding to its high-affinity receptor, triggering mast cell and basophil activation in allergic inflammation.

Air–liquid interface culture: An in vitro technique in which epithelial cells are grown at the interface of air and culture medium to model mucosal barrier differentiation.

References

1. Transcriptome Analysis Reveals Distinct Gene Expression Profiles in Eosinophilic and Noneosinophilic Chronic Rhinosinusitis with Nasal Polyps. Scientific Reports (2016).
2. Gene network approach reveals co-expression patterns in nasal and bronchial epithelium. Scientific Reports (2019).
3. Transcriptomic analysis of asthma and allergic rhinitis reveals CST1 as a biomarker of unified airways. Frontiers in Immunology (2023).
4. Eosinophilic Chronic Rhinosinusitis and Pathogenic Role of Protease. International Journal of Molecular Sciences (2023).
5. Human beta defensin-2 protects the epithelial barrier during methicillin-resistant Staphylococcus aureus infection in chronic rhinosinusitis with nasal polyps. Frontiers in Cellular and Infection Microbiology (2025).