Formation of nasal polyps: The roles of innate type 2 inflammation and deposition of fibrin.
Chronic rhinosinusitis
coagulation cascade
fibrin
fibrinolysis
mast cell
nasal polyps
tissue plasminogen activator
tryptase
Journal
The Journal of allergy and clinical immunology
ISSN: 1097-6825
Titre abrégé: J Allergy Clin Immunol
Pays: United States
ID NLM: 1275002
Informations de publication
Date de publication:
03 2020
03 2020
Historique:
received:
16
12
2019
revised:
22
01
2020
accepted:
24
01
2020
entrez:
9
3
2020
pubmed:
9
3
2020
medline:
1
12
2020
Statut:
ppublish
Résumé
Chronic rhinosinusitis (CRS) is one of the most common chronic diseases worldwide. It is a heterogeneous disease, and geographical or ethnic differences in inflammatory pattern in nasal mucosa are major issues. Tissue eosinophilia in CRS is highly associated with extensive sinus disease, recalcitrance, and a higher nasal polyp (NP) recurrence rate after surgery. The prevalence of eosinophilic CRS (ECRS) is increasing in Asian countries within the last 2 decades, and this trend appears to be occurring across the world. International consensus criteria for ECRS are required for the accurate understanding of disease pathology and precision medicine. In a multicenter large-scale epidemiological survey, the "Japanese Epidemiological Survey of Refractory Eosinophilic Chronic Rhinosinusitis study," ECRS was definitively defined when the eosinophil count in nasal mucosa is greater than or equal to 70 eosinophils/hpf (magnification, ×400), and this study proposed an algorithm that classifies CRS into 4 groups according to disease severity. The main therapeutic goal with ECRS is to eliminate or diminish the bulk of NP tissue. NPs are unique abnormal lesions that grow from the lining of the nasal and paranasal sinuses, and type 2 inflammation plays a critical role in NP development in patients with ECRS. An imbalance between protease and endogenous protease inhibitors might play a pivotal role in the initiation and exacerbation of type 2 inflammation in ECRS. Intraepithelial mast cells in NPs, showing a tryptase+, chymase- phenotype, may also enhance type 2 inflammation. Intense edema and reduced fibrosis are important histological features of eosinophilic NPs. Mucosal edema mainly consists of exuded plasma protein, and excessive fibrin deposition would be expected to contribute to the retention of proteins from capillaries and thereby perpetuate mucosal edema that may play an etiological role in NPs. Upregulation of the coagulation cascade and downregulation of fibrinolysis strongly induce abnormal fibrin deposition in nasal mucosa, and type 2 inflammation plays a central role in the imbalance of coagulation and fibrinolysis.
Identifiants
pubmed: 32145873
pii: S0091-6749(20)30116-0
doi: 10.1016/j.jaci.2020.01.027
pmc: PMC7263055
mid: NIHMS1593233
pii:
doi:
Substances chimiques
Fibrin
9001-31-4
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
740-750Subventions
Organisme : NIAID NIH HHS
ID : P01 AI145818
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI137174
Pays : United States
Informations de copyright
Copyright © 2020 American Academy of Allergy, Asthma & Immunology. All rights reserved.
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