0000000000181486

AUTHOR

Carolin Orning

showing 2 related works from this author

Digestive vacuole of Plasmodium falciparum released during erythrocyte rupture dually activates complement and coagulation.

2012

Abstract Severe Plasmodium falciparum malaria evolves through the interplay among capillary sequestration of parasitized erythrocytes, deregulated inflammatory responses, and hemostasis dysfunction. After rupture, each parasitized erythrocyte releases not only infective merozoites, but also the digestive vacuole (DV), a membrane-bounded organelle containing the malaria pigment hemozoin. In the present study, we report that the intact organelle, but not isolated hemozoin, dually activates the alternative complement and the intrinsic clotting pathway. Procoagulant activity is destroyed by phospholipase C treatment, indicating a critical role of phospholipid head groups exposed at the DV surfa…

HemeproteinsMalePain ThresholdErythrocytesImmunologyComplement Pathway AlternativePlasmodium falciparumVacuoleBiochemistryHemolysisMonocytesMicrobiologyHypesthesiaRats Sprague-DawleyPhagocytosisparasitic diseasesAnimalsHumansMalaria FalciparumBlood CoagulationLungbiologyPhospholipase CHemozoinDextran SulfatePlasmodium falciparumCell BiologyHematologyIntracellular Membranesbiology.organism_classificationComplement systemRatsAntibody opsonizationImmunologyVacuolesAlternative complement pathwaySpleenWaste disposalBlood
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Overexpression of TGF-ß1 in macrophages reduces and stabilizes atherosclerotic plaques in ApoE-deficient mice.

2011

Although macrophages represent the hallmark of both human and murine atherosclerotic lesions and have been shown to express TGF-ß1 (transforming growth factor β1) and its receptors, it has so far not been experimentally addressed whether the pleiotropic cytokine TGF-ß1 may influence atherogenesis by a macrophage specific mechanism. We developed transgenic mice with macrophage specific TGF-ß1 overexpression, crossed the transgenics to the atherosclerotic ApoE (apolipoprotein E) knock-out strain and quantitatively analyzed both atherosclerotic lesion development and composition of the resulting double mutants. Compared with control ApoE(-/-) mice, animals with macrophage specific TGF-ß1 overe…

Genetically modified mouseApolipoprotein Emedicine.medical_specialtyPathologyHistologyMouseSciencemedicine.medical_treatmentImmune CellsImmunologyAntigen-Presenting CellsMice TransgenicBiologyCardiovascularLesionTransforming Growth Factor beta1MiceApolipoproteins EModel OrganismsVascular BiologyInternal medicinemedicineGeneticsMacrophageAnimalsReceptorBiologyMice KnockoutMultidisciplinaryMacrophagesQRAnimal ModelsAtherosclerosisImmunohistochemistryPlaque AtheroscleroticCytokineEndocrinologyImmunohistochemistryMedicineFemalemedicine.symptomGene FunctionTransforming growth factorResearch ArticlePloS one
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