Search results for "Knockout"

showing 10 items of 806 documents

Influenza A virus infection inhibits the efficient recruitment of Th2 cells into the airways and the development of airway eosinophilia.

2003

Abstract Most infections with respiratory viruses induce Th1 responses characterized by the generation of Th1 and CD8+ T cells secreting IFN-γ, which in turn have been shown to inhibit the development of Th2 cells. Therefore, it could be expected that respiratory viral infections mediate protection against asthma. However, the opposite seems to be true, because viral infections are often associated with the exacerbation of asthma. For this reason, we investigated what effect an influenza A (flu) virus infection has on the development of asthma. We found that flu infection 1, 3, 6, or 9 wk before allergen airway challenge resulted in a strong suppression of allergen-induced airway eosinophil…

ChemokineEpitopes T-LymphocyteImmunoglobulin Emedicine.disease_causeMiceCell MovementInfluenza A virusImmunology and AllergyEosinophiliaChemokine CCL5LungCells CulturedChemokine CCL2Mice KnockoutMice Inbred BALB Cbiologymedicine.diagnostic_testrespiratory systemUp-Regulationmedicine.anatomical_structureInfluenza A virusChemokines CCGoblet CellsNippostrongylusmedicine.symptomBronchial HyperreactivityChemokine CCL11OvalbuminImmunologyDown-RegulationMice TransgenicCCL5VirusInterferon-gammaTh2 CellsOrthomyxoviridae InfectionsLymphopeniamedicineAnimalsLymphocyte CountPulmonary EosinophiliaStrongylida InfectionsGoblet cellMetaplasiaAllergensPeptide Fragmentsrespiratory tract diseasesMice Inbred C57BLBronchoalveolar lavageImmunologyCell Migration Inhibitionbiology.proteinInterleukin-5Journal of immunology (Baltimore, Md. : 1950)
researchProduct

An Alternative Pathway of Imiquimod-Induced Psoriasis-Like Skin Inflammation in the Absence of Interleukin-17 Receptor A Signaling

2013

Topical application of imiquimod (IMQ) on the skin of mice induces inflammation with common features found in psoriatic skin. Recently, it was postulated that IL-17 has an important role both in psoriasis and in the IMQ model. To further investigate the impact of IL-17RA signaling in psoriasis, we generated IL-17 receptor A (IL-17RA)-deficient mice (IL-17RA(del)) and challenged these mice with IMQ. Interestingly, the disease was only partially reduced and delayed but not abolished when compared with controls. In the absence of IL-17RA, we found persisting signs of inflammation such as neutrophil and macrophage infiltration within the skin. Surprisingly, already in the naive state, the skin …

ChemokineInflammationImiquimodDermatologyInterleukin-17 receptorBiochemistryMiceAdjuvants ImmunologicPsoriasismedicineAnimalsPsoriasisMacrophageMolecular BiologySkinMice KnockoutImiquimodReceptors Interleukin-17biologyInterleukin-6InterleukinsMacrophagesInterleukin-17Cell Biologymedicine.diseaseDisease Models AnimalCXCL2Neutrophil InfiltrationImmunologyAminoquinolinesbiology.proteinFemaleTumor necrosis factor alphamedicine.symptomSignal Transductionmedicine.drugJournal of Investigative Dermatology
researchProduct

Thy-1 (CD90) regulates the extravasation of leukocytes during inflammation.

2010

Human Thy-1 (CD90) has been shown to mediate adhesion of inflammatory cells to activated microvascular endothelial cells via interaction with Mac-1 (CD11b/CD18) in vitro. Since there are no data showing the physiological relevance of Thy-1 for the recruitment of inflammatory cells in vivo, different inflammation models were investigated in Thy-1-deficient mice and littermate controls. In thioglycollate-induced peritonitis, the number of neutrophils and monocytes was significantly diminished in Thy-1-deficient mice. During acute lung inflammation, the extravasation of eosinophils and monocytes into the lung was significantly reduced in Thy-1-deficient mice. Moreover, during chronic lung infl…

ChemokineMice 129 StrainNeutrophilsmedicine.medical_treatmentT-LymphocytesImmunologyInflammationCD18In Vitro TechniquesPeritonitisMonocytesMiceCell MovementCell AdhesionLeukocytesImmunology and AllergyMedicineAnimalsHumansCD90Thy-1InflammationMice KnockoutTransplantation Chimerabiologybusiness.industryInterleukinsEndothelial CellsPneumoniaExtravasationTransplantationEosinophilsMice Inbred C57BLCytokineIntegrin alpha MImmunologybiology.proteinThy-1 Antigensmedicine.symptomChemokinesbusinessextravasationPeptide HydrolasesEuropean journal of immunology
researchProduct

Toll-like receptor 2 is dispensable for acquired host immune resistance to Candida albicans in a murine model of disseminated candidiasis

2004

Previous work by our group showed that Toll-like receptor 2 (TLR2) is essential for activation of innate immunity, playing a major role in the response of macrophages to Candida albicans, triggering cytokine and chemokine expression, and therefore TLR2 -/- mice are more susceptible to systemic primary candidiasis. In this work, we used a murine model of systemic C. albicans infection, in which resistance to reinfection with virulent wild-type cells is induced by prior exposure of mice to a low-virulence agerminative strain of C. albicans (primary sublethal infection), to study the influence of TLR2 gene deletion on (i) the ability to develop an acquired resistance upon vaccination; (ii) the…

Chemokinemedicine.medical_treatmentImmunologyReceptors Cell SurfaceMicrobiologyMicrobiologyInterferon-gammaMiceCandida albicansmedicineAnimalsCandida albicansAntibodies FungalMice KnockoutToll-like receptorMembrane GlycoproteinsInnate immune systembiologyTumor Necrosis Factor-alphaToll-Like ReceptorsCandidiasisbiology.organism_classificationDisseminated CandidiasisInterleukin-12Immunity InnateToll-Like Receptor 2Corpus albicansMice Inbred C57BLTLR2Infectious DiseasesCytokineImmunoglobulin GImmunologybiology.proteinCytokinesMicrobes and Infection
researchProduct

Toll-like receptor-2 is essential in murine defenses against Candida albicans infections

2004

In this work, we studied the role of toll-like receptor-2 (TLR2) in murine defenses against Candida albicans. TLR2-deficient mice experimentally infected intraperitoneally (i.p.) or intravenously (i.v.) in vivo had very significant impaired survival compared with that of control mice. In vitro production of TNF-alpha and macrophage inhibitory protein-2 (MIP-2) by macrophages from TLR2-/- mice in response to yeasts and hyphae of C. albicans were significantly lower (80% and 40%, respectively; P <0.05) than production by macrophages from wild-type mice. This impaired production of TNF-alpha and MIP-2 probably contributed to the 41% decreased recruitment of neutrophils to the peritoneal cavity…

Chemokinemedicine.medical_treatmentPhagocytosisChemokine CXCL2ImmunologyHyphaeCell CountReceptors Cell SurfaceMicrobiologyMicrobiologyMicePhagocytosisIn vivoCandida albicansmedicineAnimalsMacrophageCandida albicansCells CulturedMice KnockoutToll-like receptorMembrane GlycoproteinsbiologyTumor Necrosis Factor-alphaToll-Like ReceptorsCandidiasisFlow Cytometrybiology.organism_classificationImmunity InnateToll-Like Receptor 2Corpus albicansMice Inbred C57BLDisease Models AnimalInfectious DiseasesCytokineMacrophages Peritonealbiology.proteinChemokinesReactive Oxygen SpeciesMicrobes and Infection
researchProduct

TLR3-induced activation of mast cells modulates CD8+ T-cell recruitment.

2005

AbstractMast cells play an important role in host defense against various pathogens, but their role in viral infection has not been clarified in detail. dsRNA, synthesized by various types of viruses and mimicked by polyinosinic-polycytidylic acid (poly(I:C)) is recognized by Toll-like receptor 3 (TLR3). In this study, we demonstrate that poly(I:C) injection in vivo potently stimulates peritoneal mast cells to up-regulate a number of different costimulatory molecules. Therefore, we examined the expression and the functional significance of TLR3 activation in mast cells. Mast cells express TLR3 on the cell surface and intracellularly. After stimulation of mast cells with poly(I:C) and Newcas…

Chemokinevirusesmedicine.medical_treatmentImmunologyNewcastle disease virusReceptors Cell SurfaceBiologyCD8-Positive T-LymphocytesBiochemistryMicemedicineCytotoxic T cellAnimalsMast CellsPhosphorylationPeritoneal CavityMice KnockoutInnate immune systemMembrane GlycoproteinsToll-Like ReceptorsCell BiologyHematologymedicine.diseaseMast cellImmunity InnateCell biologyToll-Like Receptor 3Up-RegulationMice Inbred C57BLChemotaxis Leukocytemedicine.anatomical_structureCytokinePoly I-CTLR3ImmunologyMast cell sarcomabiology.proteinCytokinesCD8Blood
researchProduct

p53 is involved in regulation of the DNA repair gene O6-methylguanine-DNA methyltransferase (MGMT) by DNA damaging agents

1998

The DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) is inducible by genotoxic stress. MGMT induction results from transcriptional activation of the MGMT gene which is a specific response to DNA damage. A possible factor involved in triggering MGMT induction might be p53, because both p53 and MGMT are activated by DNA breaks. To study the effect of p53 on induction of the MGMT gene, we compared the presence of functional wild-type (wt) and mutant p53 with MGMT expression level in various mouse fibroblasts and rat hepatoma cell lines upon genotoxic treatment. Cells which responded to ionizing radiation (IR) by MGMT induction displayed functional p53, whereas in cells not expr…

Chloramphenicol O-AcetyltransferaseCancer ResearchMethyltransferaseDNA RepairDNA damageDNA repairRecombinant Fusion ProteinsBiologyTransfectionDNA methyltransferaseDNA AntisenseGene Expression Regulation EnzymologicMiceO(6)-Methylguanine-DNA MethyltransferaseLiver Neoplasms ExperimentalGene expressionDNA Repair ProteinTumor Cells CulturedGeneticsAnimalsCancer epigeneticsPromoter Regions GeneticneoplasmsMolecular BiologyCell NucleusMice KnockoutCell Cycle3T3 CellsTransfectionGenes p53Molecular biologydigestive system diseasesRatsCancer researchTumor Suppressor Protein p53DNA DamageOncogene
researchProduct

The Bile Acid Receptor GPBAR-1 (TGR5) Modulates Integrity of Intestinal Barrier and Immune Response to Experimental Colitis

2011

Background GP-BAR1, a member G protein coupled receptor superfamily, is a cell surface bile acid-activated receptor highly expressed in the ileum and colon. In monocytes, ligation of GP-BAR1 by secondary bile acids results in a cAMP-dependent attenuation of cytokine generation. Aims To investigate the role GP-BAR1 in regulating intestinal homeostasis and inflammation-driven immune dysfunction in rodent models of colitis. Methods Colitis was induced in wild type and GP-BAR1−/− mice by DSS and TNBS administration. Potential GP-BAR1 agonists were identified by in silico screening and computational docking studies. Results GP-BAR1−/− mice develop an abnormal morphology of colonic mucous cells a…

Cholera ToxinCD14Biophysicslcsh:MedicineInflammationGastroenterology and HepatologyBiologyLigandsBiochemistryPermeabilityReceptors G-Protein-CoupledTight JunctionsMiceCrohn DiseaseCiprofloxacinMolecular Cell BiologymedicineAnimalsUlcerative ColitisIntestinal MucosaProtein PrecursorsBiomacromolecule-Ligand InteractionsColitislcsh:ScienceReceptorBiologyMice KnockoutMultidisciplinaryIntestinal permeabilityHaptoglobinsPhysicsInflammatory Bowel Diseaselcsh:RImmunityZonulinColitisFlow Cytometrymedicine.diseaseMolecular biologyG protein-coupled bile acid receptorImmunologyTLR4Medicinelcsh:Qmedicine.symptomCytometryResearch ArticlePLoS ONE
researchProduct

EphrinB2 controls vessel pruning through STAT1-JNK3 signalling

2014

Angiogenesis produces primitive vascular networks that need pruning to yield hierarchically organized and functional vessels. Despite the critical importance of vessel pruning to vessel patterning and function, the mechanisms regulating this process are not clear. Here we show that EphrinB2, a well-known player in angiogenesis, is an essential regulator of endothelial cell death and vessel pruning. This regulation depends upon phosphotyrosine-EphrinB2 signalling repressing c-jun N-terminal kinase 3 activity via STAT1. JNK3 activation causes endothelial cell death. In the absence of JNK3, hyaloid vessel physiological pruning is impaired, associated with abnormal persistence of hyaloid vessel…

Chromatin ImmunoprecipitationCell SurvivalAngiogenesisImmunoblottingRegulatorFluorescent Antibody TechniqueNeovascularization PhysiologicGeneral Physics and AstronomyEphrin-B2Persistent Hyperplastic Primary VitreousIn Vitro TechniquesBiologyBioinformaticsMicrophthalmiaArticleGeneral Biochemistry Genetics and Molecular BiologyNeovascularizationMiceMitogen-Activated Protein Kinase 10Human Umbilical Vein Endothelial CellsmedicineAnimalsHumansImmunoprecipitationInvolution (medicine)Pruning (decision trees)Cell ProliferationMice KnockoutMultidisciplinaryNeovascularization PathologicfungiEndothelial CellsRetinal VesselsGeneral ChemistryFlow Cytometrymedicine.diseaseCell biologyEndothelial stem cellSTAT1 Transcription Factornervous systemPersistent hyperplastic primary vitreousGene Knockdown Techniquescardiovascular systemmedicine.symptomSignal TransductionNature Communications
researchProduct

In vitro P-glycoprotein efflux inhibition by atypical antipsychotics is in vivo nicely reflected by pharmacodynamic but less by pharmacokinetic chang…

2011

Abstract Background P-glycoprotein (P-gp), an efflux transporter of the blood–brain barrier, limits the access of multiple xenobiotics to the central nervous system (CNS). Thus drug-dependent inhibition, induction or genetic variation of P-gp impacts drug therapy. Methods We investigated atypical antipsychotics and their interaction with P-gp. Amisulpride, clozapine, N-desmethylclozapine, olanzapine, and quetiapine were assessed in vitro on their inhibitory potential and in vivo on their disposition in mouse serum and brain, and behaviourally on the RotaRod test. In vivo wildtype (WT) and mdr1a/1b double knockout mice (mdr1a/1b (−/−, −/−); KO) were investigated. Results In rhodamine 123 eff…

Clinical BiochemistryIn Vitro TechniquesPharmacologyToxicologyBlood–brain barrierBiochemistryRhodamine 123Rotarod performance testMiceBehavioral Neurosciencechemistry.chemical_compoundPharmacokineticsIn vivoCell Line TumormedicineAnimalsRhodamine 123ATP Binding Cassette Transporter Subfamily B Member 1Biological PsychiatryClozapineP-glycoproteinMice KnockoutPharmacologybiologyReceptors Dopamine D2Protein Transportmedicine.anatomical_structurechemistryRotarod Performance Testbiology.proteinDopamine AntagonistsEffluxAntipsychotic Agentsmedicine.drugPharmacology Biochemistry and Behavior
researchProduct