TY - JOUR
T1 - Advances in the knowledge of the underlying airway remodeling mechanisms in chronic rhinosinusitis based on the endotypes
T2 - A review
AU - Lee, Kijeong
AU - Tai, Junhu
AU - Lee, Sang Hag
AU - Kim, Tae Hoon
N1 - Funding Information:
Funding: This research was supported by the Basic Science Research Program, National Research Foundation of Korea, funded by the Ministry of Science and Technology and the Ministry of Science, ICT and Future Planning (2017R1A2B2003575, NRF-2020R1A2C1006398), the Ministry of Science and ICT (2020R1C1C1012288), Korea, under the ICT Creative Consilience program (IITP-2020– 0018190011001) supervised by the IITP (Institute for Information and Communications Technology Planning and Evaluation), and the Korea Health Technology R&D Project (HI17C0387), Korea Health Industry Development Institute (KHIDI), and the Ministry of Health and Welfare. This research was also supported by a Korea University grant and a grant from Korea University Medical Center and Anam Hospital, Seoul, Republic of Korea.
Publisher Copyright:
© 2021 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2021/1/2
Y1 - 2021/1/2
N2 - 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.
AB - 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.
KW - Airway remodeling
KW - Chronic rhinosinusitis
KW - Endotypes
KW - Tissue remodeling
UR - http://www.scopus.com/inward/record.url?scp=85099949067&partnerID=8YFLogxK
U2 - 10.3390/ijms22020910
DO - 10.3390/ijms22020910
M3 - Review article
C2 - 33477617
AN - SCOPUS:85099949067
SN - 1661-6596
VL - 22
SP - 1
EP - 16
JO - International journal of molecular sciences
JF - International journal of molecular sciences
IS - 2
M1 - 910
ER -