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Seite 1 von 62 Ergebnisse
Oxygen matters: hypoxia as a pathogenic mechanism in rhinosinusitis.
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The airway epithelium is the first place, where a defense mechanism is initiated against environmental stimuli. Mucociliary transport (MCT), which is the defense mechanism of the airway and the role of airway epithelium as mechanical barriers are essential in innate immunity. To maintain normal
Overexpression of hypoxia-inducible factor 1α is associated with neutrophilic inflammation in chronic rhinosinusitis with nasal polyps.
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[Expression of hypoxia inducible factor-1α in chronic rhinosinusitis and the relationship with mucin secretion].
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OBJECTIVE
To investigate the expression of hypoxia inducible factor-1α (HIF-1α) in chronic rhinosinusitis (CRS) and relationship with mucin MUC5AC, MUC5B secretion.
METHODS
The expression of HIF-1α, MUC5AC and MUC5B were measured by immunohistochemistry (IHC), Western Blot and reverse transcription
Hypoxia in paranasal sinuses of patients with chronic sinusitis with or without the complication of nasal allergy.
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OBJECTIVE
In order to elucidate the pathogenesis of the radiologic opacity of the sinuses frequently observed in patients with allergic rhinitis, the mechanisms underlying their sinus mucosal swelling were studied clinically.
METHODS
We confirmed the presence of hypoxia in inflamed sinuses and
Hypoxia induced chemokine expression in nasal epithelial cells: development of an in vitro model for chronic rhinosinusitis.
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Chronic rhinosinusitis (CRS) is defined as an inflammatory condition involving the paranasal sinuses and the lining of the nasal passages that persists longer than 12 weeks. It is one of the most common chronic diseases today, affecting up to 15% of the adult population in the Western world with a
Hypoxia-mediated mechanism of MUC5AC production in human nasal epithelia and its implication in rhinosinusitis.
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BACKGROUND
Excessive mucus production is typical in various upper airway diseases. In sinusitis, the expression of MUC5AC, a major respiratory mucin gene, increases. However, the mechanisms leading to mucus hypersecretion in sinusitis have not been characterized. Hypoxia due to occlusion of the
The effect of hypoxia and cycloxygenase inhibitors on nasal polyp derived fibroblasts.
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OBJECTIVE
The pathogenesis of chronic rhinosinusitis with nasal polyposis is unknown. Chronic inflammation along with local tissue hypoxia may effect polyp's growth. Activation of Cycloxygenases may also be involved. COX-2 up-regulates in response to different stimuli including hypoxia. Its
Vγ1⁺ γδT Cells Are Correlated With Increasing Expression of Eosinophil Cationic Protein and Metalloproteinase-7 in Chronic Rhinosinusitis With Nasal Polyps Inducing the Formation of Edema.
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OBJECTIVE
We have found that expression of γδT cells is increased in pathological mucosa of chronic rhinosinusitis with nasal polyps (CRSwNP) compared with normal nasal mucosa. This increase is correlated with the infiltration of eosinophils in CRSwNP. Here, we investigated the expression of γδT
[Physiology of the sinuses. Physiopathology of sinusitis].
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Ventilation and drainage are the two essential intrinsic functions of the sinus. Both of them are dependent upon the permeability of the ostium, whose caliber is extremely variable with respect to anatomical factors, and dynamic factors associated with the vasomotricity of the mucous membrane. In
Role of hypoxia-inducible factor-1α expression in regulatory T cells on nasal polypogenesis.
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OBJECTIVE
Hypoxia-inducible factor-1α (HIF-1α) is considered as a key molecule in regulating Th17:regulatory T-cells (Tregs) balance. The aims of this study were to investigate whether HIF-1α is associated with the RORγ (RAR-related orphan receptor gamma) expression of Tregs in nasal polyps and to
Hypoxia regulates IL-17A secretion from nasal polyp epithelial cells.
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Hypoxia creates a microenvironment conducive to polypogenesis by regulating immune responses of the nasal polyp (NP) epithelium. We explored the immunocompetence of NP and control epithelial cells in response to hypoxia, to investigate potential relationships with polypogenesis. Three groups of
[High mobility group box1 contributes to hypoxia-induced barrier dysfunction of nasal epithelial cells].
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Objective:To investigated the promotion of high mobility group box1 (HMGB1) under hypoxia, and determined the regulatory role of HMGB1 on the barrier function of nasal epithelial cells.Method:Primary nasal epithelial cells (NECs) collected from patients with septal deviation were cultured at
Role of hypoxia in inflammatory upper airway disease.
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OBJECTIVE
Hypoxia is a potent stimulus for inflammation and remodeling. Hypoxia develops in chronic sinusitis as shown via tissue oxygen concentrations and colonization with obligate anaerobes. This hypoxia reflects occlusion of the sinus ostia and thereby failure of transepithelial oxygenation,
Hypoxia stimulates inflammatory and fibrotic responses from nasal-polyp derived fibroblasts.
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OBJECTIVE
Chronic sinusitis is primarily an inflammatory disorder characterized by hyperplasia of immune cells and sinus tissue. Nasal mucosal swelling or polyps can occlude the sinus ostia, decreasing the level of oxygen available to the sinus tissue. Hypoxia in many diseases results in increased
[Fungal sinusitis. Report of four cases].
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Fungal sinusitis has a nonspecific clinical presentation, is refractory to standard medical treatment and may produce expansion and erosion of the sinus wall. Various factors have been implicated in the development of fungal sinusitis: anatomical factors in the osteomeatal complex, tissular hypoxia,
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