Search results for "inflammation"

showing 10 items of 2662 documents

Exercise intensity and markers of inflammation during and after (neo-) adjuvant cancer treatment.

2021

Exercise training has been hypothesized to lower the inflammatory burden for patients with cancer, but the role of exercise intensity is unknown. To this end, we compared the effects of high-intensity (HI) and low-to-moderate intensity (LMI) exercise on markers of inflammation in patients with curable breast, prostate and colorectal cancer undergoing primary adjuvant cancer treatment in a secondary analysis of the Phys-Can randomized trial (NCT02473003). Sub-group analyses focused on patients with breast cancer undergoing chemotherapy. Patients performed 6 months of combined aerobic and resistance exercise on either HI or LMI during and after primary adjuvant cancer treatment. Plasma taken …

0301 basic medicineMaleCancer Researchmedicine.medical_specialtyColorectal cancerEndocrinology Diabetes and Metabolismmedicine.medical_treatmentBreast NeoplasmsGastroenterologylaw.invention03 medical and health sciences0302 clinical medicineEndocrinologyBreast cancerRandomized controlled triallawProstateInternal medicinemedicineHumansExerciseInflammationChemotherapybiologybusiness.industryC-reactive proteinCancermedicine.diseaseExercise Therapy030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisExercise intensitybiology.proteinFemalebusinessBiomarkersEndocrine-related cancer
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CD16+ Macrophages Mediate Fibrosis in Inflammatory Bowel Disease.

2017

Background and Aims Fibrosis is a common complication of Crohn's disease [CD], and is related to dysregulated tissular repair following inflammation, in which macrophages play a central role. We have previously observed that STAT6-/- mice present delayed mucosal recovery after 2,4,6-trinitrobenzenesulfonic acid [TNBS]-induced colitis due to a deficiency in reparatory interleukin-4 [IL4]/STAT6-dependent M2 macrophages, which can be reverted by the exogenous transfer of this cell type. In the present study, we analyse the role of STAT6-dependent macrophages in intestinal fibrosis. Methods Colitis was induced by weekly intra-rectal administration of TNBS [6 weeks] to STAT6-/- mice and wild-typ…

0301 basic medicineMaleCell CountInflammatory bowel diseaseMiceCrohn DiseaseFibrosisMacrophageIntestinal MucosaCells CulturedMice Knockouteducation.field_of_studyMice Inbred BALB Cintegumentary systemGastroenterologyGeneral MedicineColitisColonic NeoplasmsFemalemedicine.symptomMannose ReceptorAdultAdolescentColonPopulationInflammationReceptors Cell SurfaceCD1603 medical and health sciencesYoung AdultProto-Oncogene Proteinsparasitic diseasesmedicineAnimalsHumansLectins C-TypeColitiseducationInterleukin 4business.industryMacrophagesReceptors IgGmedicine.diseaseFibrosisWnt Proteins030104 developmental biologyMannose-Binding LectinsTrinitrobenzenesulfonic AcidImmunologyInterleukin-4businessSTAT6 Transcription FactorJournal of Crohn'scolitis
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General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation.

2016

Relapsing-remitting multiple sclerosis (MS)(2) is characterized by phases of acute neuroinflammation followed by spontaneous remission. Termination of inflammation is accompanied by an influx of regulatory T cells (Tregs).(3) The molecular mechanisms responsible for directing Tregs into the inflamed CNS tissue, however, are incompletely understood. In an MS mouse model we show that the stress kinase general control non-derepressible 2 (GCN2),(4) expressed in T cells, contributes to the resolution of autoimmune neuroinflammation. Failure to recover from acute inflammation was associated with reduced frequencies of CNS-infiltrating Tregs. GCN2 deficient Tregs displayed impaired migration to a…

0301 basic medicineMaleChemokineEncephalomyelitis Autoimmune ExperimentalTime FactorsT cellImmunologyInflammationSpontaneous remissionMice TransgenicCCL2Protein Serine-Threonine KinasesT-Lymphocytes RegulatoryStatistics Nonparametric03 medical and health sciencesMice0302 clinical medicineCell MovementmedicineImmunology and AllergyAnimalsAnnexin A5NeuroinflammationbiologyKinaseMultiple sclerosisBrainEndothelial Cellsmedicine.diseaseFlow CytometryPeptide FragmentsMice Inbred C57BLDisease Models Animal030104 developmental biologymedicine.anatomical_structureNeurologyAstrocytesImmunologybiology.proteinDisease ProgressionCytokinesFemaleMyelin-Oligodendrocyte GlycoproteinNeurology (clinical)medicine.symptom030215 immunologyJournal of neuroimmunology
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Protective effects of polyphenol-rich infusions from carob (Ceratonia siliqua) leaves and cladodes of Opuntia ficus-indica against inflammation assoc…

2017

IF 2.759; International audience; In the present study, we have investigated the effects of polyphenol-rich infusions from carob leaves and OFI-cladodes on inflammation associated with obesity and dextran sulfate sodium (DSS)-induced ulcerative colitis in Swiss mice. In vitro studies revealed that aqueous extracts of carob leaves and OFI-cladodes exhibited anti-inflammatory properties marked by the inhibition of IL-6, TNF-α and nitric oxide (NO) production in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells concomitant with NF-κβ nucleus translocation inhibition. For in vivo investigations, Swiss male mice were subjected to control or high fat diet (HFD). At the 8th week after the start …

0301 basic medicineMaleDSS colitisCarob leavesAdipose tissueInflammationBiologyPharmacologyDiet High-FatGalactansHFD obesityNitric oxideCell LineMannans03 medical and health scienceschemistry.chemical_compoundMicefoodSwiss micePlant GumsmedicineAnimalsObesityColitisAcute colitisPharmacologyInflammationIntestinal permeabilityOFI-CladodesDose-Response Relationship DrugDextran Sulfate[ SDV.SP.PHARMA ] Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyOpuntiaPolyphenolsFabaceaeGeneral Medicinemedicine.diseaseColitisUlcerative colitisfood.food3. Good healthPlant LeavesCeratonia siliquaAqueous extract030104 developmental biologychemistry[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacologymedicine.symptomInflammation MediatorsBiomedicinepharmacotherapy = Biomedecinepharmacotherapie
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Blimp1 Prevents Methylation of Foxp3 and Loss of Regulatory T Cell Identity at Sites of Inflammation

2018

Summary Foxp3+ regulatory T (Treg) cells restrict immune pathology in inflamed tissues; however, an inflammatory environment presents a threat to Treg cell identity and function. Here, we establish a transcriptional signature of central nervous system (CNS) Treg cells that accumulate during experimental autoimmune encephalitis (EAE) and identify a pathway that maintains Treg cell function and identity during severe inflammation. This pathway is dependent on the transcriptional regulator Blimp1, which prevents downregulation of Foxp3 expression and “toxic” gain-of-function of Treg cells in the inflamed CNS. Blimp1 negatively regulates IL-6- and STAT3-dependent Dnmt3a expression and function …

0301 basic medicineMaleEncephalomyelitis Autoimmune ExperimentalBlimp1CNS2Regulatory T cellInflammationchemical and pharmacologic phenomenaBiologyT-Lymphocytes RegulatoryGeneral Biochemistry Genetics and Molecular BiologyArticleepigenetic regulationDNA Methyltransferase 3AEpigenesis Genetic03 medical and health sciencesGenomic ImprintingMice0302 clinical medicineImmune systemDownregulation and upregulationmedicineAnimalsEpigeneticsDNA (Cytosine-5-)-Methyltransferaseslcsh:QH301-705.5Regulation of gene expressionInterleukin-6FOXP3Forkhead Transcription FactorsDNA methyltransferaseshemic and immune systemsDNA Methylation3. Good healthCell biologyddc:Mice Inbred C57BL030104 developmental biologymedicine.anatomical_structureregulatory T cellslcsh:Biology (General)inflammationFoxp3DNA methylationFemalePositive Regulatory Domain I-Binding Factor 1medicine.symptomCNS030217 neurology & neurosurgeryCell Reports
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Fast direct neuronal signaling via the IL-4 receptor as therapeutic target in neuroinflammation.

2018

Ongoing axonal degeneration is thought to underlie disability in chronic neuroinflammation, such as multiple sclerosis (MS), especially during its progressive phase. Upon inflammatory attack, axons undergo pathological swelling, which can be reversible. Because we had evidence for beneficial effects of T helper 2 lymphocytes in experimental neurotrauma and discovered interleukin-4 receptor (IL-4R) expressed on axons in MS lesions, we aimed at unraveling the effects of IL-4 on neuroinflammatory axon injury. We demonstrate that intrathecal IL-4 treatment during the chronic phase of several experimental autoimmune encephalomyelitis models reversed disease progression without affecting inflamma…

0301 basic medicineMaleEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisEncephalomyelitisInflammation03 medical and health sciencesMice0302 clinical medicinemedicineAnimalsHumansAxonReceptorNeuroinflammationAdministration IntranasalInflammationNeuronsbusiness.industryMultiple sclerosisExperimental autoimmune encephalomyelitisTranslation (biology)General Medicinemedicine.diseaseAxonsReceptors Interleukin-4030104 developmental biologymedicine.anatomical_structurenervous systemInterleukin-4medicine.symptombusinessNeuroscience030217 neurology & neurosurgeryLocomotionScience translational medicine
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Oxidative and endoplasmic reticulum stress is impaired in leukocytes from metabolically unhealthy vs healthy obese individuals.

2017

BACKGROUND: Oxidative stress and inflammation are related to obesity, but the influence of metabolic disturbances on these parameters and their relationship with endoplasmic reticulum (ER) stress is unknown. Therefore, this study was performed to evaluate whether metabolic profile influences ER and oxidative stress in an obese population with/without comorbidities. SUBJECTS AND METHODS: A total of 113 obese patients were enrolled in the study; 29 were metabolically healthy (MHO), 53 were metabolically abnormal (MAO) and 31 had type 2 diabetes (MADO). We assessed metabolic parameters, proinflammatory cytokines (TNF alpha and IL-6), mitochondrial and total reactive oxygen species (ROS) produc…

0301 basic medicineMaleEndocrinology Diabetes and MetabolismMedicine (miscellaneous)Blood Pressuremedicine.disease_causeBody Mass Index0302 clinical medicineLeukocytesEndoplasmic Reticulum Chaperone BiPchemistry.chemical_classificationMetabolic SyndromeNutrition and DieteticsMiddle AgedEndoplasmic Reticulum StressCytokinesFemalemedicine.symptomOxidation-ReductionAdultmedicine.medical_specialtyBlotting Western030209 endocrinology & metabolismInflammationOxidative phosphorylation03 medical and health sciencesYoung AdultInsulin resistanceInternal medicinemedicineHumansObesityAgedDyslipidemiasInflammationReactive oxygen speciesObesity Metabolically Benignbusiness.industryEndoplasmic reticulummedicine.diseaseOxidative Stress030104 developmental biologyEndocrinologychemistryMetabolic syndromeInsulin ResistancebusinessReactive Oxygen SpeciesBody mass indexOxidative stressInternational journal of obesity (2005)
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Prolonged sleep restriction induces changes in pathways involved in cholesterol metabolism and inflammatory responses

2016

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0301 basic medicineMaleEpidemiologyPhysiologychemistry.chemical_compoundinsufficient sleep0302 clinical medicineHigh-density lipoproteinFinlandSleep restrictionGENERAL-POPULATIONINSULIN-RESISTANCEeducation.field_of_studyMultidisciplinarytulehdusCARDIOVASCULAR RISKGLUCOSE-METABOLISMta3142Chronic inflammationMiddle AgedSleep in non-human animals3. Good healthSleep deprivationCholesterolMetabolomeFemalemedicine.symptomAdultmedicine.medical_specialtyACUTE-PHASE RESPONSELIVER-X-RECEPTORSPopulationBiologyta3111Articlesleep restriction03 medical and health sciencesInsulin resistanceMetabolic DiseasesInternal medicinemedicineMetabolomeHumansCORONARY-HEART-DISEASEeducationLiver X receptorDyslipidaemiasAgedCASSETTE TRANSPORTER G1Gene Expression Profilingta1182ta3121medicine.diseaseSleep deprivation030104 developmental biologyEndocrinologychemistryinflammationcholesterol metabolismSleep Deprivation3111 BiomedicineGene expressionHIGH-DENSITY-LIPOPROTEIN030217 neurology & neurosurgeryBlood Chemical AnalysisScientific Reports
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Disease severity in patients with visceral leishmaniasis is not altered by co-infection with intestinal parasites

2017

Visceral leishmaniasis (VL) is a neglected tropical disease that affects the poorest communities and can cause substantial morbidity and mortality. Visceral leishmaniasis is characterized by the presence of Leishmania parasites in the spleen, liver and bone marrow, hepatosplenomegaly, pancytopenia, prolonged fever, systemic inflammation and low body mass index (BMI). The factors impacting on the severity of VL are poorly characterized. Here we performed a cross-sectional study to assess whether co-infection of VL patients with intestinal parasites influences disease severity, assessed with clinical and haematological data, inflammation, cytokine profiles and BMI. Data from VL patients was s…

0301 basic medicineMaleIMPACTPhysiologyHepatosplenomegalySystemic inflammationPathology and Laboratory MedicineTHERAPYSeverity of Illness IndexBody Mass Index0302 clinical medicineIntestinal ParasitesBone MarrowZoonosesImmune PhysiologyMedicine and Health SciencesIntestinal Diseases ParasiticHELMINTH INFECTIONSLeishmaniasisImmune ResponseInnate Immune SystembiologyCoinfectionlcsh:Public aspects of medicineASCARIASIS11 Medical And Health SciencesHematologyPancytopenia3. Good healthInfectious DiseasesCytokinesLeishmaniasis Visceralmedicine.symptomLife Sciences & BiomedicineHepatomegalyResearch ArticleNeglected Tropical DiseasesAdultlcsh:Arctic medicine. Tropical medicineAdolescentlcsh:RC955-962030231 tropical medicineImmunology03 medical and health sciencesYoung AdultSigns and SymptomsDONOVANIDiagnostic MedicineTropical MedicineHOOKWORMSeverity of illnessmedicineParasitic DiseasesAnimalsHumansParasitesInflammationScience & TechnologyProtozoan InfectionsINTERFERON-GAMMAbusiness.industryPublic Health Environmental and Occupational HealthTropical diseaseBiology and Life SciencesLeishmaniasislcsh:RA1-127006 Biological SciencesMolecular DevelopmentINTERLEUKIN-10Leishmaniabiology.organism_classificationmedicine.diseaseTropical Diseases030104 developmental biologyVisceral leishmaniasisCross-Sectional StudiesLogistic ModelsCase-Control StudiesCo-InfectionsImmune SystemImmunologySplenomegalyUNDERNUTRITIONParasitologyEthiopiabusinessParasitic Intestinal DiseasesSpleenDevelopmental Biology
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Chronic skin inflammation leads to bone loss by IL-17-mediated inhibition of Wnt signaling in osteoblasts

2016

Item does not contain fulltext Inflammation has important roles in tissue regeneration, autoimmunity, and cancer. Different inflammatory stimuli can lead to bone loss by mechanisms that are not well understood. We show that skin inflammation induces bone loss in mice and humans. In psoriasis, one of the prototypic IL-17A-mediated inflammatory human skin diseases, low bone formation and bone loss correlated with increased serum IL-17A levels. Similarly, in two mouse models with chronic IL-17A-mediated skin inflammation,K14-IL17A(ind)andJunB(Deltaep), strong inhibition of bone formation was observed, different from classical inflammatory bone loss where osteoclast activation leads to bone deg…

0301 basic medicineMaleInflammationModels BiologicalOsteocytesBone resorptionEpithelium03 medical and health sciences0302 clinical medicineOsteoclastOsteogenesismedicineAnimalsHumansPsoriasisCell LineageBone ResorptionWnt Signaling PathwaySkin030203 arthritis & rheumatologyInflammationOsteoblastsChemistryInnate lymphoid cellInterleukin-17Wnt signaling pathwayOsteoblastGeneral MedicineMiddle AgedMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureGene Expression RegulationOsteocyteImmunologyChronic DiseaseCancer researchFemaleInterleukin 17medicine.symptomInflammatory diseases Radboud Institute for Molecular Life Sciences [Radboudumc 5]Science Translational Medicine
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