nasal polyps/protease

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Emerging Role of Proteases in the Pathogenesis of Chronic Rhinosinusitis with Nasal Polyps.

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Chronic rhinosinusitis with nasal polyps (CRSwNP) is a heterogeneous upper airway disease with multiple etiologies. Clinically, CRSwNP can be classified into either eosinophilic or non-eosinophilic subtypes. The eosinophilic phenotype of CRSwNP is widely thought to be highly associated with

Significance of lysosomal proteases; cathepsins B and H in maxillary mucosa and nasal polyp with non-atopic chronic inflammation.

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Tissue extracts from maxillary mucosa (MM) and nasal polyp (NP) with non-atopic chronic inflammation were applied to DEAE-Sepharose, and hydrolytic activity of lysosomal proteases (cathepsins B and H) was measured by the fluorometric assay. Hydrolytic activity of cathepsins B and H in MM, of which

Thrombin and activated coagulation factor X stimulate the release of cytokines and fibronectin from nasal polyp fibroblasts via protease-activated receptors.

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BACKGROUND Nasal epithelial cells and infiltrating eosinophils express tissue factor, and high thrombin activity and excess fibrin deposition are found in nasal secretion and in nasal polyp from patients with chronic rhinosinusitis with nasal polyp (CRSwNP). Activated coagulation factors play

Development of a mouse model of eosinophilic chronic rhinosinusitis with nasal polyp by nasal instillation of an Aspergillus protease and ovalbumin.

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One subtype of chronic rhinosinusitis with nasal polyps (CRSwNP) is characterized by the development of a T-helper type 2 (Th2) response and eosinophilic infiltration. Here, we aimed to establish an eosinophilic CRSwNP murine model, which would be essential to understand the underlying pathogenesis

Protease-dependent activation of nasal polyp epithelial cells by airborne fungi leads to migration of eosinophils and neutrophils.

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CONCLUSIONS Proteases in fungi interact with nasal epithelial cells and enhance the production of inflammatory cytokines in vitro. These cytokines induced the migration of eosinophils and neutrophils. Protease-activated receptors (PARs) might also play a role in the process of epithelial cell

Tissue and Exosomal Serine Protease Inhibitors Are Significantly Overexpressed in Chronic Rhinosinusitis With Nasal Polyps.

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Histochemical and immunohistochemical characteristics of mast cells in nasal polyps.

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In surgically excised nasal polyps, most epithelial mast cells were formalin sensitive, chloroacetate esterase (CAE) negative, and chymase negative. Thus, this represents a population of mast cells not identified by staining for CAE. On the other hand, most stromal mast cells were formalin resistant

The epithelium-derived inflammatory mediators of chronic rhinosinusitis with nasal polyps.

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Introduction: Chronic rhinosinusitis with nasal polyps (CRSwNP) is an inflammatory airway disease characterized as tight junction loosening, inflammation, and mucosal remodeling. Epithelial cells form a barrier against allergens, bacteria, and proteases, and can also trigger or enhance the

Partial purification and characterization of the tissue plasminogen activator in nasal mucosa and nasal polyp.

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Tissue plasminogen activator was partially purified from the inferior turbinate and nasal polyp, and its biochemical properties were investigated. Similar TPA peak positions were seen in the gel filtration chromatography of both tissues, and the molecular weight was approximately 65,000, which was

Distribution, subtype population, and IgE positivity of mast cells in chronic rhinosinusitis with nasal polyps.

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Chronic rhinosinusitis with nasal polyps (CRSwNP) has been categorized into 2 subtypes in the Asian population: eosinophilic chronic rhinosinusitis (ECRS; similar to CRSwNP in Western countries) and non-ECRS (characterized by inflammation dominated by T-helper cell type 1). The pathogenesis of

Airborne fungi induce nasal polyp epithelial cell activation and Toll-like receptor expression.

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BACKGROUND The nasal epithelium is the first barrier encountered by airborne allergens and is an active participant in airway inflammation. Fungi have been increasingly recognized as important pathogens in sinusitis and airway diseases. The aim of the study was to evaluate fungal protease activity

Tissue factor and tissue factor pathway inhibitor in nasal mucosa and nasal secretions of chronic rhinosinusitis with nasal polyp.

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BACKGROUND Activation of the coagulation system with an increase in thrombin generation is involved in the pathogenesis of tissue remodeling in chronic rhinosinusitis (CRS). Tissue factor (TF) is an important protein for initiation of the extrinsic coagulation pathway, and TF pathway inhibitor

Role of TLRs in the production of chemical mediators in nasal polyp fibroblasts by fungi.

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OBJECTIVE Fibroblasts are major supporting cells in nasal mucosa and can induce inflammatory process with recruitment of inflammatory cells. Airborne fungi have been suggested as an etiologic factor of chronic rhinosinusitis (CRS). The aim of this study was to investigate the interaction between

Epithelial genes in chronic rhinosinusitis with and without nasal polyps.

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BACKGROUND Genetic studies on chronic inflammatory diseases have resulted in an emphasis on the epithelial interface with the environment and the genes that influence this interaction. This study examines the expression of key epithelial genes implicated in the pathogenesis of other inflammatory

Expression of protease-activated receptors in allergic fungal rhinosinusitis.

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BACKGROUND The etiology of the intense inflammatory response showed by patients with allergic fungal rhinosinusitis (AFRS) remains a mystery. Potential sources of this inflammation may include fungal proteases. Protease-activated receptors (PARs) are components of the innate immune response that are

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