0000000000437517

AUTHOR

Jula Huppert

showing 4 related works from this author

Pro-inflammatory effects of interleukin-17A on vascular smooth muscle cells involve NAD(P)H- oxidase derived reactive oxygen species.

2010

T cells are known for their contribution to the inflammatory element of atherosclerosis. Recently, it has been demonstrated that the Th17 derived cytokine IL-17 is involved in the pro-inflammatory response of vascular smooth muscle cells (VSMC). The aim of the present study was to examine whether reactive oxygen species (ROS) might be involved in this context. The effect of IL-17A on ROS generation was examined using the fluorescent dye 2′7′-dichlorodihydrofluorescein (H<sub>2</sub>DCF) in primary murine VSMC. IL-17A induced an increase in H<sub>2</sub>DCF fluorescence in VSMC, and this effect was blocked by the NAD(P)H-oxidase inhibitor apocynin and siRNA targeting …

Vascular smooth musclePhysiologymedicine.medical_treatmentAorta Thoracicmedicine.disease_causep38 Mitogen-Activated Protein KinasesMuscle Smooth Vascularchemistry.chemical_compoundMiceCell MovementmedicineAnimalsEnzyme InhibitorsRNA Small InterferingCells Culturedchemistry.chemical_classificationReactive oxygen speciesNADPH oxidaseMembrane GlycoproteinsbiologyInterleukin-17AcetophenonesNADPH OxidasesCell DifferentiationMolecular biologyMice Inbred C57BLOxidative StressCytokinechemistryBiochemistryNAD(P)H oxidaseNADPH Oxidase 4ApocyninNADPH Oxidase 2cardiovascular systembiology.proteinCytokinesNAD+ kinaseCardiology and Cardiovascular MedicineReactive Oxygen SpeciesOxidative stressJournal of vascular research
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Cellular mechanisms of IL-17-induced blood-brain barrier disruption.

2009

Recently T-helper 17 (Th17) cells were demonstrated to disrupt the blood-brain barrier (BBB) by the action of IL-17A. The aim of the present study was to examine the mechanisms that underlie IL-17A-induced BBB breakdown. Barrier integrity was analyzed in the murine brain endothelial cell line bEnd.3 by measuring the electrical resistance values using electrical call impedance sensing technology. Furthermore, in-cell Western blots, fluorescence imaging, and monocyte adhesion and transendothelial migration assays were performed. Experimental autoimmune encephalomyelitis (EAE) was induced in C57BL/6 mice. IL-17A induced NADPH oxidase- or xanthine oxidase-dependent reactive oxygen species (ROS)…

1303 BiochemistryEncephalomyelitisOccludin10263 Institute of Experimental ImmunologyBiochemistryMice0302 clinical medicineEnzyme InhibitorsCell Line Transformed0303 health sciencesMice Inbred BALB CNADPH oxidasebiologyTight junctionExperimental autoimmune encephalomyelitisInterleukin-17AzepinesT-Lymphocytes Helper-InducerCell biologyEndothelial stem cellBlood-Brain Barrier1305 BiotechnologyBiotechnologyXanthine OxidaseMyosin light-chain kinaseEncephalomyelitis Autoimmune ExperimentalDown-Regulation610 Medicine & healthNaphthalenes03 medical and health sciences1311 GeneticsOccludinGeneticsmedicine1312 Molecular BiologyAnimalsMolecular BiologyMyosin-Light-Chain KinaseNeuroinflammation030304 developmental biologyEndothelial CellsMembrane ProteinsNADPH Oxidasesmedicine.diseaseMolecular biologyAntibodies NeutralizingOxidative Stressbiology.protein570 Life sciences; biologyReactive Oxygen Species030217 neurology & neurosurgeryFASEB journal : official publication of the Federation of American Societies for Experimental Biolog
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IL-17 controls central nervous system autoimmunity through the intestinal microbiome

2021

Interleukin-17A- (IL-17A) and IL-17F-producing CD4(+) T helper cells (T(H)17 cells) are implicated in the development of chronic inflammatory diseases, such as multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). T-H 17 cells also orchestrate leukocyte invasion of the central nervous system (CNS) and subsequent tissue damage. However, the role of IL-17A and IL-17F as effector cytokines is still confused with the encephalitogenic function of the cells that produce these cytokines, namely, T-H 17 cells, fueling a long-standing debate in the neuroimmunology field. Here, we demonstrated that mice deficient for IL-17A/F lose their susceptibility to EAE, which…

0301 basic medicineCentral Nervous SystemMaleEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisreceptorImmunologyCentral nervous system610 Medicine & healthGut flora10263 Institute of Experimental Immunologymedicine.disease_causeAutoimmunityinterleukin-1703 medical and health sciencesMice0302 clinical medicinemedicinecytokineAnimalsHumanscnst-cellsMice Knockout2403 Immunologybiologygut microbiotaMultiple sclerosisExperimental autoimmune encephalomyelitisGeneral MedicineFecal Microbiota Transplantationneutralizationmedicine.diseasebiology.organism_classificationAdoptive Transfer3. Good healthGut EpitheliumGastrointestinal Microbiome030104 developmental biologyNeuroimmunologymedicine.anatomical_structureImmunology2723 Immunology and Allergy570 Life sciences; biologyTh17 CellssequencesFemaleInterleukin 17030217 neurology & neurosurgery
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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
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