Search results for "ASTHMA"

showing 10 items of 860 documents

Efficacy and tolerability of anti-immunoglobulin E therapy with omalizumab in patients with concomitant allergic asthma and persistent allergic rhini…

2004

Background: Anti-IgE therapy could be particularly beneficial for patients with concomitant disease as it targets a common factor in both diseases. The aim of this study was to evaluate the efficacy and safety of omalizumab in patients with concomitant moderate-to-severe asthma and persistent allergic rhinitis. Methods: This multicentre, randomized, double-blind, parallel-group, placebocontrolled trial evaluated the safety and efficacy of omalizumab. A total of 405 patients (12–74 years) with a stable treatment (‡ 400 lg budesonide Turbuhaler � )a nd‡ 2 unscheduled medical visits for asthma during the past year or ‡ 3 during the past 2 years were enrolled. Patients received omalizumab (‡ 0.…

Budesonidemedicine.medical_specialtyAllergybiologybusiness.industryImmunologyOmalizumabPlacebomedicine.diseaseImmunoglobulin ESurgeryTolerabilityConcomitantInternal medicinemedicinebiology.proteinImmunology and Allergybusinessmedicine.drugAsthmaAllergy
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Budesonide/formoterol for maintenance and reliever therapy in the management of moderate to severe asthma.

2008

The Global Initiative for Asthma (GINA) guidelines aim at improving asthma control and preventing future risk. For patients with moderate to severe asthma an inhaled corticosteroid (ICS) or an ICS/long-acting beta2-agonist (LABA) combination with a short-acting beta2-agonist (SABA) as reliever is recommended. Despite the availability of effective maintenance therapies, a large proportion of patients still fail to achieve guideline-defined asthma control, and overuse of SABA reliever medication at the expense of ICS is commonly observed. New simplified treatment approaches may offer a solution and assist physicians to achieve overall asthma control. One such treatment approach, which is reco…

Budesonidemedicine.medical_specialtyExacerbationImmunologySeverity of Illness IndexPharmacotherapyimmune system diseasesFormoterol FumarateSeverity of illnessAdministration InhalationmedicineImmunology and AllergyAnimalsHumansAnti-Asthmatic AgentsIntensive care medicineBudesonideAsthmaInhalationbusiness.industrymedicine.diseaseAsthmarespiratory tract diseasesBudesonide/formoterolEthanolaminesPhysical therapyDrug Therapy CombinationFormoterolbusinessmedicine.drugAllergy
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Asthma bronchiale: neue Erkenntnisse und Entwicklungen

2011

In mild asthma low-dose steroid inhalation treatment reduces severe exacerbations and exacerbation associated loss of lung function. In patients with mild asthma, symptom-driven use of a combination of inhaled steroid and short-acting beta-2-sympathomimetics in a single inhaler is feasible. In moderate and severe asthma the fixed combination of formoterol and budesonide can be used a maintenance therapy but also as treatment of acute symptoms. Monotherapy with long-acting beta 2-sympathomimetics should be completely avoided. Long-acting anticholinergic drugs are equally efficacious as long-acting beta-2-sympathomimetics, but have not yet been approved for use in patients with asthma. The co…

Budesonidemedicine.medical_specialtyExacerbationInhalationbusiness.industryInhalerGeneral Medicinemedicine.diseaseInhaled steroidrespiratory tract diseasesMaintenance therapyInternal medicinemedicineFormoterolbusinessmedicine.drugAsthmaDMW - Deutsche Medizinische Wochenschrift
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Safety Considerations of Inhaled Corticosteroids in the Elderly

2014

Inhaled corticosteroids (ICSs) are widely used in the treatment of patients with chronic obstructive pulmonary diseases. However, high-dose regimens and long-term use of ICSs have the potential to cause a variety of local and systemic side effects such as candidiasis, cataracts, glaucoma, and osteoporosis. The use of ICSs can also be associated with the risk of bone fractures, diabetes mellitus and pneumonia. These ICS-related side effects are of particular importance in elderly patients due to the presence of comorbidities and age-related behavioral, cognitive, and psychological problems, which can all interact with inhaled treatment. We reviewed the available literature on the clinically …

Budesonidemedicine.medical_specialtyOsteoporosisSettore MED/10 - Malattie Dell'Apparato RespiratorioFluticasone propionatePulmonary Disease Chronic ObstructivePharmacotherapyCataractsAdrenal Cortex HormonesDiabetes mellitusAdministration InhalationmedicineHumansPharmacology (medical)asthma corticosteroidsIntensive care medicineAgedCOPDbusiness.industrymedicine.diseaseAsthmaPneumoniaTreatment OutcomePhysical therapyGeriatrics and Gerontologybusinessmedicine.drugDrugs & Aging
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Patients' perceptions of well-being using a guided self-management plan in asthma

2004

Summary Asthma can place considerable restrictions on the health-related quality of life of asthma patients and their families; this burden may be greatest when symptoms are not adequately controlled. The Symbicort® Adjustable Maintenance Dosing Programme, consisting of studies from several different countries, compared a guided self-management plan that allows adjustable maintenance dosing using budesonide/formoterol in a single inhaler (Symbicort) with fixed dosing. Quality of life was assessed in three countries, using asthma-specific and generic questionnaires. Clinically relevant improvements in mean quality of life scores were observed from the beginning to the end of the 1-month run-…

Budesonidemedicine.medical_specialtySelf-managementbusiness.industryInhalerGeneral Medicinemedicine.diseaseBudesonide/formoterolQuality of lifemedicinePhysical therapyFormoterolDosingbusinessAsthmamedicine.drugInternational Journal of Clinical Practice
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Cylindromatosis (Cyld) gene mutation in T cells promotes the development of an IL-9-dependent allergic phenotype in experimental asthma

2016

Cylindromatosis (CYLD) is a ubiquitously expressed deubiquitinating enzyme which removes activating ubiquitin residues from important signaling molecules of the NF-κB pathway. In CYLDex7/8 transgenic mice, a naturally occurring short isoform (sCYLD) is overexpressed in the absence of full length CYLD, leading to excessive NF-κB activity. Herein, we investigated the impact of the CYLDex7/8 mutation selectively in T cells on the development of experimental allergic airway disease induced by sensitization and challenge with ovalbumin. Compared with their wildtype littermates, mice bearing the T cell-specific mutation (CD4+CYLDex7/8) display stronger eosinophilia and mucus production in the lun…

CD4-Positive T-Lymphocytes0301 basic medicineSkin Neoplasmsmedicine.medical_treatmentT cellImmunologyGene mutationImmunoglobulin Emedicine.disease_causeTh9 cellsDeubiquitinating enzymeMice03 medical and health sciencesNeoplastic Syndromes HereditaryHypersensitivitymedicineAnimalsHumansSensitizationMice KnockoutMutationbiologyTumor Suppressor ProteinsInterleukin-9Cylindromatosis (turban tumor syndrome) geneIL-9AsthmaDeubiquitinating Enzyme CYLDEosinophilsMice Inbred C57BLMucusOvalbumin030104 developmental biologymedicine.anatomical_structureCytokineModels AnimalMutationImmunologybiology.proteinCellular Immunology
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The role of Th1/Th2 polarization in mucosal immunity

2002

Mucosal immunity relies on the delicate balance between antigen responsiveness and tolerance. The polarization of T helper cells plays a key role in maintaining or disrupting this equilibrium.

CD4-Positive T-LymphocytesChemistryModels ImmunologicalCell PolarityGeneral MedicineTh1 CellsInflammatory Bowel DiseasesAsthmaGeneral Biochemistry Genetics and Molecular BiologyTh2 polarizationTh2 CellsAntigenImmunityImmunologyAnimalsHumansImmunity MucosalMucosal immunityNature Medicine
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Asthmatic changes in mice lacking T-bet are mediated by IL-13

2005

Mice with a targeted deletion of the T-bet gene exhibit spontaneous airway hyperresponsiveness (AHR), airway inflammation, enhanced recovery of T(h)2 cytokines from bronchoalveolar lavage fluid, sub-epithelial collagen deposition and myofibroblast transformation. Here we analyze the mechanisms responsible for the chronic airway remodeling observed in these mice. CD4+ T cells isolated from the lung of T-bet-deficient mice were spontaneously activated CD44(high)CD69(high) memory T cells, with a typical T(h)2 cytokine profile. Neutralization of IL-13 but not IL-4 resulted in amelioration of AHR in airways of mice lacking T-bet. IL-13 blockade also led to reduced eosinophilia and decreased vime…

CD4-Positive T-LymphocytesImmunologychemical and pharmacologic phenomenaVimentinLymphocyte ActivationSmad7 ProteinMiceTransforming Growth Factor betamedicineAnimalsVimentinImmunology and AllergyEosinophiliaSmad3 ProteinLungCells CulturedMice KnockoutInterleukin-13Lungbiologymedicine.diagnostic_testChemistryCD69hemic and immune systemsGeneral MedicineTransforming growth factor betaFibroblastsrespiratory systemActinsAsthmarespiratory tract diseasesDNA-Binding ProteinsMice Inbred C57BLBronchoalveolar lavagemedicine.anatomical_structureInterleukin 13ImmunologyTrans-Activatorsbiology.proteinCytokinesInterleukin-4medicine.symptomT-Box Domain ProteinsImmunologic MemoryMyofibroblastTranscription FactorsInternational Immunology
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The receptor NLRP3 is a transcriptional regulator of TH2 differentiation.

2015

The receptor NLRP3 is involved in the formation of the NLRP3 inflammasome that activates caspase-1 and mediates the release of interleukin 1β (IL-1β) and IL-18. Whether NLRP3 can shape immunological function independently of inflammasomes is unclear. We found that NLRP3 expression in CD4(+) T cells specifically supported a T helper type 2 (TH2) transcriptional program in a cell-intrinsic manner. NLRP3, but not the inflammasome adaptor ASC or caspase-1, positively regulated a TH2 program. In TH2 cells, NLRP3 bound the Il4 promoter and transactivated it in conjunction with the transcription factor IRF4. Nlrp3-deficient TH2 cells supported melanoma tumor growth in an IL-4-dependent manner and …

CD4-Positive T-LymphocytesInflammasomesImmunologyBlotting WesternBiologyInterleukin 21MiceTh2 CellsCell Line TumorNLR Family Pyrin Domain-Containing 3 ProteinImmunology and AllergyCytotoxic T cellAnimalsIL-2 receptorPromoter Regions GeneticInterleukin 3Oligonucleotide Array Sequence AnalysisMice KnockoutCD40integumentary systemReverse Transcriptase Polymerase Chain ReactionZAP70Gene Expression ProfilingCell DifferentiationNeoplasms ExperimentalAsthmaCell biologyGene Expression Regulation NeoplasticMice Inbred C57BLInterleukin 10Interferon Regulatory FactorsInterleukin 12biology.proteinNIH 3T3 CellsTrans-ActivatorsFemaleInterleukin-4Carrier ProteinsProtein BindingSignal TransductionNature immunology
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Local blockade of IL-6R signaling induces lung CD4+ T cell apoptosis in a murine model of asthma via regulatory T cells.

2007

We previously reported high levels of the soluble form of the IL-6R (sIL-6R) in the airways of asthmatic subjects. Here, we analyzed the IL-6R effects on Th2 cell survival in the lung by locally antagonizing sIL-6R-mediated trans-signaling with a designer fusion protein (gp130-Fc) as well as IL-6R signaling with an antibody against the gp80 unit of the IL-6R (alphaIL-6R) in a murine model of asthma after ovalbumin peptide (OVA) sensitization and challenge. Blockade of the sIL-6R led to a significant decrease in inflammatory cells by an apoptosis-independent mechanism. In contrast, local treatment with alphaIL-6R antibodies that also block signaling via the membrane-bound IL-6R (mIL-6R) led …

CD4-Positive T-LymphocytesSTAT3 Transcription FactorOvalbuminT cellRecombinant Fusion ProteinsImmunologyGene ExpressionApoptosisBiologyT-Lymphocytes RegulatoryAntibodiesInterleukin 21MicemedicineCytokine Receptor gp130Immunology and AllergyCytotoxic T cellAnimalsIL-2 receptorPhosphorylationLungMice Inbred BALB CInterleukin-6FOXP3Forkhead Transcription FactorsGeneral MedicineT lymphocyterespiratory systemReceptors Interleukin-6AsthmaCoculture TechniquesImmunoglobulin Fc FragmentsDisease Models Animalmedicine.anatomical_structureApoptosisImmunologyCancer researchFemaleImmunizationSignal transductionBronchoalveolar Lavage FluidSignal TransductionInternational immunology
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