0000000000205063

AUTHOR

Nuria Carpena

showing 4 related works from this author

Immunosuppression, peripheral inflammation and invasive infection from endogenous gut microbiota activate retinal microglia in mouse models

2016

Although its actual role in the progression of degenerative processes is not fully known, the persistent activated state of retinal microglia and the concurrent secretion of inflammatory mediators may contribute to neuronal death and permanent vision loss. Our objective was to determine whether non-ocular conditions (immunosuppression and peripheral inflammation) could lead to activation of retinal microglia. Mouse models of immunosuppression induced by cyclophosphamide and/or peripheral inflammation by chemically induced sublethal colitis in C57BL/6J mice were used. Retinal microglia morphology, spatial distribution and complexity, as well as MHCII and CD11b expression levels were determin…

0301 basic medicinemedicine.medical_treatmentImmunologyInflammationMicrobiology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDownregulation and upregulationVirologymedicineColitisMicrogliabiologyImmunosuppressionRetinalmedicine.diseaseTLR2030104 developmental biologymedicine.anatomical_structureIntegrin alpha MchemistryImmunologybiology.proteinmedicine.symptom030217 neurology & neurosurgeryMicrobiology and Immunology
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β-Adrenoceptors differentially regulate vascular tone and angiogenesis of rat aorta via ERK1/2 and p38

2014

β-Adrenoceptors (β-ARs) modulate ERK1/2 and p38 in different cells, but little is known about the contribution of these signaling pathways to the function of β-ARs in vascular tissue. Immunoblotting analysis of rat aortic rings, primary endothelial (ECs) and smooth muscle cells (SMCs) isolated from aorta showed that β-AR stimulation with isoprenaline activated p38 in aortic rings and in both cultured cell types, whereas it had a dual effect on ERK1/2 phosphorylation, decreasing it in ECs while increasing it in SMCs. These effects were reversed by propranolol, which by itself increased p-ERK1/2 in ECs. Isoprenaline β-AR mediated vasodilation of aortic rings was potentiated by the ERK1/2 inhi…

Malemedicine.medical_specialtyEndotheliumPhysiologyAngiogenesisVasodilator AgentsAdrenergic beta-AntagonistsMyocytes Smooth MuscleNeovascularization PhysiologicAorta ThoracicStimulationVasodilationFibroblast growth factorp38 Mitogen-Activated Protein KinasesMuscle Smooth VascularInternal medicineIsoprenalinemedicine.arteryReceptors Adrenergic betamedicineAnimalsHumansRats WistarMitogen-Activated Protein Kinase 1PharmacologyMatrigelAortaMitogen-Activated Protein Kinase 3business.industryAdrenergic beta-AgonistsPropranololRatsVasodilationHEK293 Cellsmedicine.anatomical_structureEndocrinologycardiovascular systemMolecular MedicineEndothelium Vascularbusinessmedicine.drugVascular Pharmacology
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TLR2 modulates gut colonization and dissemination of Candida albicans in a murine model

2016

Invasive candidiasis often arises from translocation of endogenous yeasts from the gastrointestinal tract to the bloodstream. Here we describe that both wild type and TLR2−/− mice strains, orally administered with Candida albicans yeasts, display similar sustained high level of gut colonization when oral antibacterial treatment is present, while removal of antibiotic treatment causes a progressive clearance of yeasts in control but not in TLR2−/− mice. Fungal invasion of internal organs, following immunosuppression of colonized mice, was increased in TLR2−/− mice. These results point out to a role of TLR2 in gut protection against colonization and endogenous invasion by C. albicans. This wo…

0301 basic medicinemedicine.drug_classFarmacología030106 microbiologyImmunologyAntibioticsEndogenyGut colonizationMicrobiologyMicrobiology03 medical and health sciencesImmunosuppressed miceCandida albicansmedicineTLR2AnimalsCandidiasis InvasiveColonizationCandida albicansMice KnockoutGastrointestinal tractbiologyWild typebiology.organism_classificationToll-Like Receptor 2Corpus albicansGastrointestinal TractMice Inbred C57BLTLR2030104 developmental biologyInfectious DiseasesImmunologyDisease SusceptibilityMicrobes and Infection
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Retinal microglia are activated by systemic fungal infection

2014

Purpose: To determine whether systemic fungal infection could cause activation of retinal microglia and therefore could be potentially harmful for patients with retinal degenerative diseases. Methods: Activation of retinal microglia was measured in a model of sublethal invasive candidiasis in C57BL/6J mice by (i) confocal immunofluorescence and (ii) flow cytometry analysis, using anti-CD11b, anti-Iba1, anti-MHCII and anti-CD45 antibodies. Results: Systemic fungal infection causes activation of retinal microglia, with phenotypic changes in morphology, surface markers expression, and microglial re-location in retinal layers. Conclusions: As an excessive or prolonged microglial activation may …

Retinal Ganglion CellsSystemic mycosisFarmacologíaBiología CelularAxonal TransportRetinachemistry.chemical_compoundMicemedicineAnimalsMicroglial activationInflammationMicroscopy ConfocalMicrogliabusiness.industryRetinal DegenerationCandidiasisRetinalFlow CytometryImmunohistochemistryMice Inbred C57BLDisease Models Animalmedicine.anatomical_structurechemistryImmunologyChristian ministryFemaleMicrogliabusinessInfection
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