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eosinophilia/protease
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Sivu 1 alkaen 95 tuloksia
Stimulation of protease-activated receptor-2 inhibits airway eosinophilia, hyperresponsiveness and bronchoconstriction in a murine model of allergic inflammation.
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1. An emerging body of evidence indicates that PGE(2) has a privileged anti-inflammatory role within the airways. Stimulants of protease-activated receptor-2 (PAR(2)) inhibit airway smooth muscle tone in vitro and in vivo predominantly via cyclooxygenase (COX)-dependent generation of prostaglandin
Interplay Between the IL-33/ST2 Axis and Bone Marrow ILC2s in Protease Allergen-Induced IL-5-Dependent Eosinophilia
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Background: Eosinophils develop from CD34+ progenitor cells in the bone marrow under the influence of interleukin (IL)-5. Several cell types produce IL-5, including type 2 innate lymphoid cells (ILC2s). The alarmin cytokine IL-33 is known to activate ILC2s in mucosal tissues, but
Serine protease inhibitors nafamostat mesilate and gabexate mesilate attenuate allergen-induced airway inflammation and eosinophilia in a murine model of asthma.
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BACKGROUND
Serine proteases such as mast cell tryptase and certain allergens are important in the pathogenesis of allergic inflammation of asthma.
OBJECTIVE
We sought to investigate the effects of serine protease inhibitors nafamostat mesilate (FUT), gabexate mesilate (FOY), and ulinastatin (UTI) on
IL-33-mediated innate response and adaptive immune cells contribute to maximum responses of protease allergen-induced allergic airway inflammation.
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How the innate and adaptive immune systems cooperate in the natural history of allergic diseases has been largely unknown. Plant-derived allergen, papain, and mite allergens, Der f 1 and Der p 1, belong to the same family of cysteine proteases. We examined the role of protease allergens in the
Epicutaneous Allergic Sensitization by Cooperation between Allergen Protease Activity and Mechanical Skin Barrier Damage in Mice.
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Allergen sources such as mites, insects, fungi, and pollen contain proteases. Airway exposure to proteases induces allergic airway inflammation and IgE/IgG1 responses via IL-33-dependent mechanisms in mice. We examined the epicutaneous sensitization of mice to a model protease allergen, papain; the
Innate IL-17A Enhances IL-33-independent Skin Eosinophilia and IgE Response on Subcutaneous Papain Sensitization
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IL-33-activated group 2 innate lymphoid cells critically contribute to protease allergen-induced airway inflammation models. However, IL-33 is dispensable for a subcutaneous papain-induced skin inflammation model, suggesting distinct mechanisms between intranasal and subcutaneous sensitization. We
Raltegravir-induced Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) syndrome - implications for clinical practice and patient safety.
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This case report describes two severe antiretroviral drug adverse reactions that occurred in the same patient. A 55-year-old HIV-positive African woman received a single epidural triamcinolone injection for pain relief of postherpetic neuralgia. Forty-one days later, she developed severe iatrogenic
Development of Aspergillus protease with ovalbumin-induced allergic chronic rhinosinusitis model in the mouse.
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BACKGROUND
Chronic rhinosinusitis (CRS) is a multifactorial inflammatory disease. Particularly, eosinophilic CRS is often recalcitrant to treatment, so an appropriate animal model is required to evaluate the pathogenesis of, and to develop therapies for, recalcitrant eosinophilic CRS. This study
IL-33, IL-25 and TSLP contribute to development of fungal-associated protease-induced innate-type airway inflammation.
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Certain proteases derived from house dust mites and plants are considered to trigger initiation of allergic airway inflammation by disrupting tight junctions between epithelial cells. It is known that inhalation of proteases such as house dust mite-derived Der p1 and/or papaya-derived papain caused
Integrated innate mechanisms involved in airway allergic inflammation to the serine protease subtilisin.
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Proteases are recognized environmental allergens, but little is known about the mechanisms responsible for sensing enzyme activity and initiating the development of allergic inflammation. Because usage of the serine protease subtilisin in the detergent industry resulted in an outbreak of
Absence of late airway response despite increased airway responsiveness and eosinophilia in a murine model of asthma.
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In asthmatics an immediate asthmatic response occurs after antigen provocation. Furthermore, asthmatic patients display airway hyperresponsiveness, accompanied by airway eosinophilia. In some patients late asthmatic responses can be detected. Many controversies still exist about the relations
A rare and severe cutaneous adverse effect of telaprevir: drug rash with eosinophilia and systemic symptoms.
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Telaprevir is a specific inhibitor of the hepatitis C (HCV) serine protease 3. Cutaneous side effects have been reported with telaprevir. Drug reaction with eosinophilia and systemic symptoms (DRESS) is a rare yet severe adverse drug-induced reaction characterized by exfoliative dermatitis and
Echinococcus multilocularis metacestode metabolites contain a cysteine protease that digests eotaxin, a CC pro-inflammatory chemokine.
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In many helminthic infections, eotaxin, a CC-chemokine, triggers the mobilization of eosinophils, thus, contributing to an elevated blood and periparasitic eosinophil level. Following an experimental intraperitoneal infection of C57BL6 mice with Echinococcus multilocularis metacestodes, however, we
First case of drug rash eosinophilia and systemic symptoms due to boceprevir.
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Boceprevir and telaprevir are 2 specific inhibitors of the hepatitis C (HCV) serine protease 3. Cutaneous side effects have been reported with high frequency, essentially rash, and dry skin. We report a case of drug rash with eosinophilia and systemic symptoms (DRESS) due to boceprevir. A
Subcutaneous Allergic Sensitization to Protease Allergen Is Dependent on Mast Cells but Not IL-33: Distinct Mechanisms between Subcutaneous and Intranasal Routes.
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Protease activity of papain, a plant-derived occupational allergen homologous to mite major allergens, is essential to IgE/IgG1 production and lung eosinophilia induced by intranasal papain administration in mice, and IL-33 contributes to these responses. In this work, we investigate skin and Ab
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