Search results for "Inflammation."

showing 10 items of 2627 documents

Neuroinflammation by cytotoxic T-lymphocytes impairs retrograde axonal transport in an oligodendrocyte mutant mouse.

2012

Mice overexpressing proteolipid protein (PLP) develop a leukodystrophy-like disease involving cytotoxic, CD8+ T-lymphocytes. Here we show that these cytotoxic T-lymphocytes perturb retrograde axonal transport. Using fluorogold stereotactically injected into the colliculus superior, we found that PLP overexpression in oligodendrocytes led to significantly reduced retrograde axonal transport in retina ganglion cell axons. We also observed an accumulation of mitochondria in the juxtaparanodal axonal swellings, indicative for a disturbed axonal transport. PLP overexpression in the absence of T-lymphocytes rescued retrograde axonal transport defects and abolished axonal swellings. Bone marrow tr…

Retinal Ganglion CellsProteolipid protein 1MouseCD8-Positive T-LymphocytesGranzymesMyelinMiceBone Marrow TransplantationNeuronsddc:616MultidisciplinarybiologyQRNeurodegenerative DiseasesAnimal ModelsCell biologyOligodendrogliamedicine.anatomical_structureNeurologyMedicineResearch ArticleHeterozygoteMultiple SclerosisProteolipidsScienceImmunologyMice Transgenicchemical and pharmacologic phenomenaAutoimmune DiseasesModel OrganismsmedicineAnimalsBiologyNeuroinflammationInflammationImmunityDemyelinating DisordersOligodendrocyteAxonsGranzyme BPerforinGranzymenervous systemImmune SystemImmunologyMutationAxoplasmic transportbiology.proteinClinical ImmunologyMolecular NeuroscienceT-Lymphocytes CytotoxicNeurosciencePLoS ONE
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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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The mitotic spindle protein SPAG5/Astrin connects to the Usher protein network postmitotically

2011

Abstract Background Mutations in the gene for Usher syndrome 2A (USH2A) are causative for non-syndromic retinitis pigmentosa and Usher syndrome, a condition that is the most common cause of combined deaf-blindness. To gain insight into the molecular pathology underlying USH2A-associated retinal degeneration, we aimed to identify interacting proteins of USH2A isoform B (USH2AisoB) in the retina. Results We identified the centrosomal and microtubule-associated protein sperm-associated antigen (SPAG)5 in the retina. SPAG5 was also found to interact with another previously described USH2AisoB interaction partner: the centrosomal ninein-like protein NINLisoB. Using In situ hybridization, we foun…

Retinal degenerationGenetics and epigenetic pathways of disease [NCMLS 6]Usher syndromeBiologyPhotoreceptor cell03 medical and health sciences0302 clinical medicineMicrotubuleEvaluation of complex medical interventions Genomic disorders and inherited multi-system disorders [NCEBP 2]Retinitis pigmentosamedicineotorhinolaryngologic diseasesBasal bodylcsh:QH573-671Ganglion cell layer030304 developmental biologyGenetics0303 health sciencesRetinalcsh:CytologyResearchPathogenesis and modulation of inflammation Infection and autoimmunity [N4i 1]Cell Biologymedicine.diseaseGenetics and epigenetic pathways of disease Plasticity and memory [NCMLS 6]eye diseasesCell biologyGenetics and epigenetic pathways of disease DCN MP - Plasticity and memory [NCMLS 6]medicine.anatomical_structure030220 oncology & carcinogenesissense organs
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Bacterial and viral infections and related inflammatory responses in chronic obstructive pulmonary disease

2021

Abstract In chronic obstructive pulmonary disease (COPD) patients, bacterial and viral infections play a relevant role in worsening lung function and, therefore, favour disease progression. The inflammatory response to lung infections may become a specific indication of the bacterial and viral infections. We here review data on the bacterial–viral infections and related airways and lung parenchyma inflammation in stable and exacerbated COPD, focussing our attention on the prevalent molecular pathways in these different clinical conditions. The roles of macrophages, autophagy and NETosis are also briefly discussed in the context of lung infections in COPD. Controlling their combined response…

Review ArticleNK cells030204 cardiovascular system & hematologyAdaptive Immunitymedicine.disease_causeAutoimmunityPulmonary Disease Chronic Obstructive0302 clinical medicineNETosiPulmonary Medicine030212 general & internal medicineLungRespiratory Tract InfectionsT-lymphocytesCOPDB cellpyroptosisautoimmunityPyroptosisNETosisGeneral Medicinerespiratory systemAcquired immune systemmacrophagesmedicine.anatomical_structureautoimmunity; autophagy; B cells; dendritic cells; disability; ILCs; macrophages; NETosis; NK cells; outcome; pyroptosis; T-lymphocytesDisease Progressionoutcomemedicine.symptomSignal Transductionautophagydendritic cellILCsContext (language use)Inflammationmacrophage03 medical and health sciencesImmune systemmedicineHumansNK celldendritic cellsB cellsLungbusiness.industrymedicine.diseaseImmunity Innaterespiratory tract diseasespyroptosiILCdisabilityImmunologybusiness
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IFN-gamma-induced protein 10 is a novel biomarker of rhinovirus-induced asthma exacerbations

2007

BACKGROUND: Rhinovirus-induced acute asthma is the most frequent trigger for asthma exacerbations. OBJECTIVE: We assessed which inflammatory mediators were released from bronchial epithelial cells (BECs) after infection with rhinovirus and then determined whether they were also present in subjects with acute virus-induced asthma, with the aim to identify a biomarker or biomarkers for acute virus-induced asthma. METHODS: BECs were obtained from bronchial brushings of steroid-naive asthmatic subjects and healthy nonatopic control subjects. Cells were infected with rhinovirus 16. Inflammatory mediators were measured by means of flow cytometry with a cytometric bead array. Subjects with acute a…

RhinovirusExacerbationNF-κB Nuclear factor κBAnti-Inflammatory Agentsairway inflammationmedicine.disease_causeDexamethasoneImmunology and AllergyChemokine CCL5LungRV-16 Rhinovirus 16Cells CulturedLR Likelihood ratioRespiratory diseaseMiddle AgedFlow Cytometrymedicine.anatomical_structureBiomarker (medicine)medicine.symptomRhinovirusChemokines CXCmedicine.drugAdultAdolescentImmunologyInflammationIFN gammaArticlemedicineHumansDexamethasoneAgedAsthmaPicornaviridae InfectionsInterleukin-6Tumor Necrosis Factor-alphabusiness.industryInterleukin-8BEC Bronchial epithelial cellEpithelial CellsTCID50 Tissue culture infectious dose 50%medicine.diseaseAsthmarespiratory tract diseasesChemokine CXCL10ImmunologyIP-10 IFN-γ–induced protein 10businessBiomarkersRespiratory tract
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trans -Lycopene from tomato juice attenuates inflammatory biomarkers in human plasma samples: An intervention trial

2017

cope : To evaluate the effects of carotenoids from tomato juice (TJ) on inflammatory biomarkers, by performing a 4-week dose-response nutritional trial in a population at high cardiovascular risk. Methods and results : An open, prospective, randomized, cross-over, and controlledclinical trial was carried out with 28 volunteers (mean age 69.7 ± 3.1 years; mean BMI 31.5 ± 3.6 kg/m2) at high cardiovascular risk, which were assigned to consume daily for 4 weeks in random order: 200 mL (LD) or 400 mL (HD) of TJ, or water as a control (C), with a 21-day wash-out period between each intervention. Blood samples were collected at baseline (B) and after each intervention. Endpoints included significa…

Risk0301 basic medicinemedicine.medical_specialtyChemokinePopulationVascular Cell Adhesion Molecule-1Inflammation030204 cardiovascular system & hematologyGastroenterologyBody Mass Index03 medical and health scienceschemistry.chemical_compoundLycopene0302 clinical medicineSolanum lycopersicumFunctional FoodInternal medicinemedicineHumansObesityIntervention trialeducationCarotenoidAgedchemistry.chemical_classificationeducation.field_of_studyCross-Over Studies030109 nutrition & dieteticsbiologyAnti-Inflammatory Agents Non-SteroidalStereoisomerismMiddle AgedAtherosclerosisIntercellular Adhesion Molecule-1CarotenoidsInflammatory biomarkersLycopeneSurgeryFruit and Vegetable JuiceschemistrySpainHuman plasmabiology.proteinInflammation Mediatorsmedicine.symptomBiomarkersFollow-Up StudiesFood ScienceBiotechnologyMolecular Nutrition & Food Research
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Polymorphisms of pro-inflammatory genes and Alzheimer's disease risk: A pharmacogenomic approach.

2006

Clinically and pathologically Alzheimer's disease (AD) represents a sequential progressive neurodegenerative disorder. AD is etiologically heterogeneous and accounts for a majority of dementia in western societies. Inflammation clearly occurs in pathologically vulnerable regions of the AD brain and the search for genetic factors influencing the pathogenesis of AD has lead to the identification of numerous gene polymorphisms that might act as susceptibility modifiers. Accordingly, several reports have indicated that the risk of AD is substantially influenced by several genetic polymorphisms in the promoter region, or other untranslated regions, of genes encoding inflammatory mediators, altho…

RiskAgingDiseaseBiologyBioinformaticsPathogenesisDegenerative diseaseGeneticAlzheimer DiseaseGenetic variationmedicineDementiaSettore MED/05 - Patologia ClinicaAnimalsHumansGeneGeneticsInflammationSettore MED/04 - Patologia GeneraleGenomePolymorphism Geneticmedicine.diseasePharmacogeneticsPharmacogenomicsAlzheimer's diseaseInflammation MediatorsPharmacogenomicsAlzheimer’s diseaseDevelopmental Biology
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Therapeutic modulation of lipoprotein-associated phospholipase A2 (Lp-PLA2)

2011

Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a calcium-independent phospholipase A2 that circulates in plasma in association with lipoprotein particles, whereas in atherosclerotic plaques it is co-localized with macrophages. Lp-PLA2 generates two proinflammatory mediators, lysophosphatidylcholine and oxidized nonesterified fatty acids, which play a role in the development of atherosclerotic lesions and formation of a necrotic core, leading to more vulnerable plaques. Epidemiologic studies demonstrate that increased circulating levels of Lp-PLA2 predict an increased risk of myocardial infarction, stroke and cardiovascular mortality. Furthermore, histologic examination of diseased hum…

RiskPathologymedicine.medical_specialtycoronary-artery-diseasecardiovascular-diseasePharmacologyatherosclerotic plaqueProinflammatory cytokinechemistry.chemical_compoundPhospholipase A2cardiovascular diseaseDarapladibOximesDrug DiscoveryHyperlipidemiamedicineHumansMyocardial infarctionPharmacologyClinical Trials as Topicbiologylow-density-lipoproteinLipoprotein-associated phospholipase A2risk-assessmentCardiovascular AgentsAtherosclerosismedicine.diseaselp-pla2heart-diseaselipoproteinsLysophosphatidylcholinechemistryCardiovascular DiseasesinflammationBenzaldehydes1-Alkyl-2-acetylglycerophosphocholine Esterasebiology.proteindarapladibrheumatoid-arthritislipids (amino acids peptides and proteins)atherosclerosisfactor-acetylhydrolase activityAtherosclerosis Cardiovascular disease Darapladib Inflammation Lipoproteins Lp-PLA2.platelet-activating-factorsecondary preventionLipoprotein
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Die allergisch-hyperergische Entzündung von Haut und Gelenken unter dem Einflu\ von Hyaluronidase und Rutin

1954

Es wurde der Einflu\ von Hyaluronidase und Rutin auf die allergisch-hyperergische Entzundung der Haut und der Gelenke beim Kaninchen untersucht. Hyaluronidase allein ruft lediglich ein entzundliches odem hervor. Hyaluronidase am Ort der Antigenreinjektion appliziert fuhrt in der Haut zu einer AbschwAchung und im Gelenk zu einer VerstArkung der Entzundung. Intravenose Hyaluronidasegaben verstArken die Entzundung in der Haut, wAhrend die Arthritis keine wesentliche Beeinflussung erfAhrt. Rutin intravenos gegeben fuhrt zu einer deutlichen Herabminderung der Entzundungserscheinungen an Haut und Gelenken.

Rutinchemistry.chemical_compoundchemistrybusiness.industryHyaluronidaseMedicineInflammationGeneral Medicinemedicine.symptombusinessMolecular biologymedicine.drugZeitschrift für Die Gesamte Experimentelle Medizin
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MiR-29b antagonizes the pro-inflammatory tumor-promoting activity of multiple myeloma-educated dendritic cells

2017

Dendritic cells (DCs) have a key role in regulating tumor immunity, tumor cell growth and drug resistance. We hypothesized that multiple myeloma (MM) cells might recruit and reprogram DCs to a tumor-permissive phenotype by changes within their microRNA (miRNA) network. By analyzing six different miRNA-profiling data sets, miR-29b was identified as the only miRNA upregulated in normal mature DCs and significantly downregulated in tumor-associated DCs. This finding was validated in primary DCs co-cultured in vitro with MM cell lines and in primary bone marrow DCs from MM patients. In DCs co-cultured with MM cells, enforced expression of miR-29b counteracted pro-inflammatory pathways, includin…

STAT3 Transcription Factor0301 basic medicineCancer Researchdendritic cellDown-RegulationInflammationMice SCIDBiologyMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationBone MarrowCell Line Tumorhemic and lymphatic diseasesmicroRNAmedicineAnimalsHumanstumor immunologyMultiple myelomaCell ProliferationInflammationmicroRNA.Cell growthNF-kappa BDendritic CellsHematologySTAT3 Transcription Factormedicine.diseaseNFKB1Up-RegulationGene Expression Regulation Neoplasticmultiple myelomaMicroRNAs030104 developmental biologymedicine.anatomical_structureOncologyCancer researchOriginal ArticleFemaleBone marrowTh17medicine.symptom030215 immunology
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