Chronic rhinosinusitis (CRS) is a chronic inflammatory condition of the nasal and paranasal sinus mucosa that affects up to 10% of the population worldwide. CRS is the most representative disease of the upper respiratory tract where airway remodeling occurs, including epithelial damage, thickening of the basement membrane, fibrosis, goblet cell hyperplasia, subepithelial edema, and osteitis. CRS is divided into two phenotypes according to the presence or absence of nasal polyps: CRS with nasal polyp (CRSwNP) and CRS without nasal polyps (CRSsNP). Based on the underlying pathophysiologic mechanism, CRS is also classified as eosinophilic CRS and non-eosinophilic CRS, owing to Type 2 T helper (Th2)-based inflammation and Type 1 T helper (Th1)/Type 17 T helper (Th17) skewed immune response, respectively. Differences in tissue remodeling in CRS are suggested to be based on the clinical phenotype and endotypes; this is because fibrosis is prominent in CRSsNP, whereas edematous changes occur in CRSwNP, especially in the eosinophilic type. This review aims to summarize the latest information on the different mechanisms of airway remodeling in CRS according to distinct endotypes.

Prostaglandins (PGs) are a family of lipid compounds that are derived from arachidonic acid via the cyclooxygenase pathway, and consist of PGD₂, PGI₂, PGE₂, PGF₂, and thromboxane B₂. PGs signal through G-protein coupled receptors, and individual PGs affect allergic inflammation through different mechanisms according to the receptors with which they are associated. In this review article, we have focused on the metabolism of the cyclooxygenase pathway, and the distinct biological effect of each PG type on various cell types involved in allergic airway diseases, including asthma, allergic rhinitis, nasal polyposis, and aspirin-exacerbated respiratory disease.

Background: Epithelial barrier disruption is a crucial feature of allergic rhinitis (AR). Previous reports have indicated the role of transient receptor potential vanilloid (TRPV) 4 in regulating the intercellular junctions in various cells. However, the role of TRPV4 and its regulation by T helper 2 cell cytokines in the epithelial cells of patients with AR remains unclear. Objective: We aimed to elucidate the expression of TRPV4 in nasal epithelial cells and its cytokine-induced regulation, and to reveal its role in house dust mite-induced junction disruption in AR. Methods: The expression of TRPV4 in nasal epithelial cells was measured using real-time polymerase chain reaction, western blot, and immunohistochemical assays, and the expression levels were compared between the patients with AR and healthy controls. Altered expression of TRPV4 was induced in cultured nasal epithelial cells by stimulation of interleukin (IL) 4, IL-13, and tumor necrosis factor alpha. In addition, expression of E-cadherin and zonula occludens 1 was induced in Der p 1-stimulated epithelial cells by treatment with either a TRPV4 agonist (GSK1016790A) or a TRPV4 antagonist (RN1734). Results: TRPV4 expression was increased in epithelial cells harvested from the affected turbinates compared to those from the normal turbinates. The stimulation of cultured epithelial cells with IL-4 and IL-13 resulted in TRPV4 upregulation. Additionally, E-cadherin and zonula occludens 1 expression levels decreased in the cultured epithelial cells treated with GSK1016790A after stimulation with Der p 1, whereas Der p 1 stimulation alone showed no effect on junctional protein expression. Conclusions: Increased TRPV4 expression occurred in epithelial cells harvested from patients with AR and epithelial cells stimulated by Th2 cytokines. Decreased junctional protein expression in epithelial cells after the stimulation by house dust mite allergen with TRPV4 agonist indicates a possible role of TRPV4 in the pathogenesis of allergen-induced epithelial barrier disruption in AR.

Chronic rhinosinusitis is an upper respiratory disease during which topical drug treatment via the nasal cavity is the most actively utilized therapeutic strategy. In addition to steroids, antibiotics, and antifungal agents, which are widely used in clinical practice, research on novel topical agents to improve the bacterial biofilm or mucociliary clearance remains ongoing. Moreover, owing to the complex structure of the nasal cavity, the effects of nasal drug delivery vary depending on factors related to delivery fluid dynamics, including device, volume, and compounds. In this article, we review methods and compounds that have been applied to chronic rhinosinusitis management and introduce recent advances and future perspectives in nasal drug delivery for upper respiratory diseases.

Central compartment atopic disease (CCAD) has recently been suggested as a phenotype of chronic rhinosinusitis (CRS). This study aims to investigate the prevalence of the radiologic CCAD phenotype in CRS within a pediatric population and identify its ability to predict comorbid allergy and asthma. Computed tomography and endoscopic examination were conducted on pediatric patients with CRS either with or without nasal polyps. Allergen sensitization was determined with the multiple-allergen simultaneous test and skin prick test. Serum total immunoglobulin E (IgE), peripheral blood eosinophil percentage, and presence of asthma were also evaluated. A total of 82 pediatric patients were enrolled. Overall, 55 (67.1%) of the participants demonstrated aeroallergen sensitization, and 31 (18.9%) of the 164 sides of sinuses were radiologically defined to fit the CCAD phenotype. Patients having CRS with the CCAD phenotype had a higher prevalence of aeroallergen sensitization (87.1% vs 62.4%, P = .008), particularly house dust mite (74.2% vs 53.4%, P = .035), and a higher incidence of asthma (16.1% vs 3.8%, P = .010). Additionally, patients having CRS with the CCAD phenotype demonstrated a high serum total IgE levels (51.6% vs 30.1%, P = .023) in comparison to patients having CRS without CCAD. In pediatric CRS, the radiological CCAD phenotype was associated with allergen sensitization and asthma. Furthermore, the CCAD phenotype was associated with high serum total IgE levels, suggesting allergy etiology should be considered with this type of pediatric patients with CRS.

An association between fiber intake and allergic diseases in children has been reported; however, many studies have not been conducted to assess this association in adults. We aimed to evaluate the association between dietary fiber intake and allergic diseases (asthma, allergic rhinitis, and atopic dermatitis) among 10,479 adults using data from the Korean National Health and Nutrition Examination Survey (2010–2011). As dietary fiber intake increased, the prevalence of asthma (Q4 adjusted odds ratio (OR): 0.656; 95% confidence interval (CI): 0.48–0.91, p for trend < 0.0001) and atopic dermatitis (Q3 crude OR: 0.746; 95% CI: 0.57–0.98; Q4 adjusted OR: 0.712; 95% CI: 0.50–1.01, p for trend < 0.0001) decreased. The prevalence of allergic rhinitis (Q2 adjusted OR: 0.840; 95% CI: 0.70–1.00, p for trend < 0.0001) tended to decrease, especially in males. Subgroup analysis revealed that fiber intake reduced allergic rhinitis symptoms, including watery rhinorrhea (Q3 adjusted OR: 0.734; 95% CI: 0.55–0.97; Q4 adjusted OR: 0.722; 95% CI: 0.54–0.97) and dog allergen sensitization (Q3 adjusted OR: 0.319; 95% CI: 0.13–0.82; Q4 adjusted OR: 0.338; 95% CI: 0.13–0.86), exclusively in males. Thus, dietary fiber intake influences allergic diseases in adults, especially males.