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Review
. 2021 Jan 18;22(2):910.
doi: 10.3390/ijms22020910.

Advances in the Knowledge of the Underlying Airway Remodeling Mechanisms in Chronic Rhinosinusitis Based on the Endotypes: A Review

Affiliations
Review

Advances in the Knowledge of the Underlying Airway Remodeling Mechanisms in Chronic Rhinosinusitis Based on the Endotypes: A Review

Kijeong Lee et al. Int J Mol Sci. .

Abstract

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.

Keywords: airway remodeling; chronic rhinosinusitis; endotypes; tissue remodeling.

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Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.

Figures

Figure 1
Figure 1
Pathophysiology of epithelial remodeling (epithelial barrier disruption, goblet cell hyperplasia, and epithelial–mesenchymal transition) in chronic rhinosinusitis according to the type of inflammation (type 2 versus non-type 2) (figure created using Biorender.com).
Figure 2
Figure 2
Subepithelial remodeling (extracellular matrix deposition, fibrin deposition, basement membrane thickening, and submucosal hypertrophy) according to the type of inflammation in chronic rhinosinusitis.
Figure 3
Figure 3
Bone remodeling based on the type of inflammation (type 2 inflammation versus non-type 2 inflammation) in chronic rhinosinusitis (figure created using Biorender.com).

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