Search results for "Inflammatory cytokine"

showing 10 items of 464 documents

An Inflammatory Profile Correlates With Decreased Frequency of Cytotoxic Cells in Coronavirus Disease 2019

2020

Abstract Increased production of inflammatory cytokines and myeloid-derived suppressor cells occurs in patients with coronavirus disease 2019. These inversely correlated with perforin-expressing natural killer (NK) and CD3+ T cells. We observed a lower number of perforin-expressing NK cells in intensive care unit (ICU) patients compared with non-ICU patients, suggesting an impairment of the immune cytotoxic arm as a pathogenic mechanism.

0301 basic medicineMicrobiology (medical)medicine.medical_treatmentMDSCInflammationchemical and pharmacologic phenomenaNK cellsProinflammatory cytokineNatural killer cell03 medical and health sciences0302 clinical medicineImmune systemmedicineCytotoxic T cellcytotoxic cellcytotoxic cellsbiologybusiness.industryCOVID-19COVID-19; cytotoxic cells; inflammation; MDSC; NK cells030104 developmental biologymedicine.anatomical_structureCytokineInfectious DiseasesPerforinSettore MED/38 - PEDIATRIA GENERALE E SPECIALISTICAinflammation030220 oncology & carcinogenesisImmunologybiology.proteinMyeloid-derived Suppressor Cellmedicine.symptombusinessClinical Infectious Diseases
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Insulin Resistance in PCOS Patients Enhances Oxidative Stress and Leukocyte Adhesion: Role of Myeloperoxidase

2016

Cardiovascular diseases and oxidative stress are related to polycystic ovary syndrome (PCOS) and insulin resistance (IR). We have evaluated the relationship between myeloperoxidase (MPO) and leukocyte activation in PCOS patients according to homeostatic model assessment of IR (HOMA-IR), and have explored a possible correlation between these factors and endocrine and inflammatory parameters. This was a prospective controlled study conducted in an academic medical center. The study population consisted of 101 PCOS subjects and 105 control subjects. We divided PCOS subjects into PCOS non-IR (HOMA-IR2.5). Metabolic and anthropometric parameters, total and mitochondrial reactive oxygen species (…

0301 basic medicineMitochondrial ROSendocrine system diseasesmedicine.medical_treatment030204 cardiovascular system & hematologyPathology and Laboratory Medicinemedicine.disease_causeBiochemistryWhite Blood CellsFluorescence MicroscopyEndocrinology0302 clinical medicineAnimal CellsMedicine and Health SciencesLeukocytesInsulinImmune ResponseEnergy-Producing OrganellesMicroscopyMultidisciplinaryQRLight MicroscopyPolycystic ovaryMitochondriaOncologyMyeloperoxidaseHomeostatic model assessmentCytokinesMedicineFemaleCellular TypesCellular Structures and OrganellesInflammation MediatorsResearch ArticlePolycystic Ovary SyndromeAdultmedicine.medical_specialtyAdhesion MoleculesImmune CellsScienceImmunologyBioenergeticsBiologyResearch and Analysis MethodsProinflammatory cytokineYoung Adult03 medical and health sciencesSigns and SymptomsInsulin resistanceDiagnostic MedicineInternal medicineCell AdhesionmedicineHumansPeroxidaseInflammationDiabetic EndocrinologyBlood CellsInsulinBiology and Life SciencesCancers and Neoplasmsnutritional and metabolic diseasesCell BiologyMolecular Developmentmedicine.diseaseHormonesOxidative Stress030104 developmental biologyEndocrinologybiology.proteinInsulin ResistanceReactive Oxygen SpeciesGynecological TumorsOxidative stressDevelopmental Biology
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Necrostatin-1 Attenuates Cisplatin-Induced Nephrotoxicity Through Suppression of Apoptosis and Oxidative Stress and Retains Klotho Expression

2018

Aim: Cisplatin is an effective chemotherapeutic drug, but the application in clinical is greatly limited by its nephrotoxicity. Necrostatin-1 (Nec-1), an inhibitor of RIP1 kinase, has been reported to inhibit RIP-mediated necroptosis. The aim of this study is to detect the protective effects of Nec-1 on the nephrotoxicity of cisplatin and to investigate its renoprotection mechanism.Methods: 8-week-old male C57BL/6 mice were randomly assigned into four groups: Control, Nec-1, Cisplatin, and Cisplatin+Nec-1. Mice were treated with cisplatin with or without Nec-1 pre-treatment. Renal function, histological changes, necroptosis, and apoptotic markers were investigated. NFκB pathway related prot…

0301 basic medicineNecroptosiscisplatinnecroptosisInflammationPharmacologymedicine.disease_causeKlothoNephrotoxicityProinflammatory cytokine03 medical and health sciences0302 clinical medicinemedicineoxidative stressPharmacology (medical)KlothoOriginal ResearchCisplatinPharmacologyKidneybusiness.industrylcsh:RM1-950apoptosisdigestive system diseases030104 developmental biologymedicine.anatomical_structurelcsh:Therapeutics. Pharmacologyinflammation030220 oncology & carcinogenesismedicine.symptomNecrostatin-1businessOxidative stressmedicine.drugFrontiers in Pharmacology
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Pathogenesis of antiphospholipid syndrome: recent insights and emerging concepts

2018

Introduction: Even though our understanding of the antiphospholipid syndrome (APS) has improved tremendously over the last decades, we are still not in a position to replace symptomatic anticoagulation by pathogenesis based causal treatments. Areas covered: Recent years have provided further insights into pathogenetically relevant mechanisms. These include a differentiation of pathogenic subtypes of antiphospholipid antibodies (aPL), novel mechanisms modulating disease activity, for example, extracellular vesicles and microRNA, and novel players in pathogenesis, for example, neutrophils and neutrophil extracellular traps (NETs). Expert commentary: It is evident that aPL induce a proinflamma…

0301 basic medicineNeutrophilsImmunologyBioinformaticsExtracellular TrapsExtracellular vesiclesProinflammatory cytokinePathogenesisExtracellular VesiclesGenetic Heterogeneity03 medical and health sciences0302 clinical medicineimmune system diseasesAntiphospholipid syndromemicroRNAHumansImmunology and AllergyMedicineFetal lossBlood CoagulationComplement Activation030203 arthritis & rheumatologybusiness.industryNeutrophil extracellular trapsAntiphospholipid Syndromemedicine.diseaseMicroRNAs030104 developmental biologyAntibodies AntiphospholipidSignal transductionbusinessExpert Review of Clinical Immunology
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Regulatory T Cells Prevent Neutrophilic Infiltration of Skin during Contact Hypersensitivity Reactions by Strengthening the Endothelial Barrier

2020

The healing phase of contact hypersensitivity reactions is critically dependent on regulatory T cells (Tregs), but even the early inflammatory phase, that is, 6-24 hours after induction of a contact hypersensitivity reaction, is susceptible to Treg-mediated suppression. To investigate the underlying mechanisms, we injected Tregs before the challenge and analyzed the skin-infiltrating cells as early as 6 hours later. Early on, we found mainly neutrophils in the challenged skin, but only a few T cells. This influx of neutrophils was blocked by the injection of Tregs, indicating that they were able to prevent the first wave of leukocytes, which are responsible for starting an immune reaction. …

0301 basic medicineNeutrophilsRegulatory T cellchemical and pharmacologic phenomenaCell CommunicationPicryl ChlorideDermatologyFilaminT-Lymphocytes RegulatoryBiochemistryProinflammatory cytokineMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationNectinmedicineAnimalsHumansProtein kinase AMolecular BiologySkinChemistryChemotaxisCell BiologyCell biologyEndothelial stem cellDisease Models Animal030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisDermatitis Allergic ContactEndothelium VascularIntracellularJournal of Investigative Dermatology
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Immune-modulating effects of bevacizumab in metastatic non-small-cell lung cancer patients

2016

AbstractThe mPEBev is an anticancer regimen which combines a chemotherapy doublet, based on cisplatin and oral etoposide (mPE), with bevacizumab (mPEBev), a mAb targeting the vasculo-endothelial growth factor (VEGF). In previous studies, this regimen showed powerful anti-angiogenetic effects and significant antitumor activity in metastatic non-small-cell lung cancer (mNSCLC) patients. We also recorded the best benefit in patients exhibiting low-systemic inflammatory profile at baseline. On these bases, we hypothesized that mPEBev antitumor activity could be partially related to bevacizumab-associated immunological effects. For this reason, we performed an immunological monitoring in 59 out …

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyBevacizumabmedicine.medical_treatmentImmunologybevacizumabArticleProinflammatory cytokine03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineIn vivoInternal medicinemedicinebevacizumab lung cancer immunocytofluorimetric analysisLung cancerCisplatinChemotherapybusiness.industryCell Biologymedicine.diseaselung cancerRegimenCTL*030104 developmental biology030220 oncology & carcinogenesisImmunologyimmunocytofluorimetric analysisbevacizumab non small lung cancer immune system vegf t lymphocytesbusinessmedicine.drugCell Death Discovery
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2017

Danger associated molecular patterns (DAMPs) are released by damaged cells and trigger neuroinflammation through activation of non-specific pattern recognition receptors (PRRs), e.g. Toll-like receptors (TLRs). Since the role of TLR 2 and 4 after traumatic brain injury (TBI) is still unclear, we examined the outcome and the expression of proinflammatory mediators after experimental TBI in Tlr2/4 / and wild-type (WT) mice. Tlr2/4 / and wild-type mice were subjected to controlled cortical injury and contusion volume and brain edema formation were assessed 24 h thereafter. Expression of inflammatory markers in brain tissue was measured by quantitative PCR 15 min, 3, 6, 12, and 24 h after contr…

0301 basic medicinePathologymedicine.medical_specialtyTraumatic brain injurybusiness.industryPoison controlmedicine.diseaseProinflammatory cytokine03 medical and health sciencesTLR2030104 developmental biology0302 clinical medicineImmune systemNeurologymedicineTumor necrosis factor alphaNeurology (clinical)Receptorbusiness030217 neurology & neurosurgeryNeuroinflammationFrontiers in Neurology
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TGF-β Serum Levels in Diabetic Retinopathy Patients and the Role of Anti-VEGF Therapy.

2020

Transforming growth factor &beta

0301 basic medicinePlacental growth factorMaleVascular Endothelial Growth Factor Aserum biomarkersGastroenterologylcsh:ChemistryPathogenesischemistry.chemical_compound0302 clinical medicineTransforming Growth Factor betaMedicineMolecular Targeted Therapylcsh:QH301-705.5SpectroscopyAfliberceptAged 80 and overGeneral MedicineDiabetic retinopathyTGFComputer Science ApplicationsVascular endothelial growth factor ABiomarker (medicine)Intercellular Signaling Peptides and ProteinsFemaleTomography Optical Coherencemedicine.drugmedicine.medical_specialtyanti-VEGFAAnti-VEGFA; Diabetic retinopathy; Serum biomarkers; TGFCatalysisArticleProinflammatory cytokineInorganic Chemistry03 medical and health sciencesTGFβInternal medicineHumansPhysical and Theoretical ChemistryMolecular BiologyAgedDiabetic Retinopathybusiness.industryOrganic Chemistrymedicine.diseaseeye diseases030104 developmental biologylcsh:Biology (General)lcsh:QD1-999chemistryDiabetes Mellitus Type 2ROC Curve030221 ophthalmology & optometryGlycated hemoglobinbusinessBiomarkersInternational journal of molecular sciences
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Kinase-independent functions of RIPK1 regulate hepatocyte survival and liver carcinogenesis.

2017

The mechanisms that regulate cell death and inflammation play an important role in liver disease and cancer. Receptor-interacting protein kinase 1 (RIPK1) induces apoptosis and necroptosis via kinase-dependent mechanisms and exhibits kinase-independent prosurvival and proinflammatory functions. Here, we have used genetic mouse models to study the role of RIPK1 in liver homeostasis, injury, and cancer. While ablating either RIPK1 or RelA in liver parenchymal cells (LPCs) did not cause spontaneous liver pathology, mice with combined deficiency of RIPK1 and RelA in LPCs showed increased hepatocyte apoptosis and developed spontaneous chronic liver disease and cancer that were independent of TNF…

0301 basic medicineProgrammed cell deathLiver tumorCell SurvivalNecroptosisMice TransgenicBiologyChronic liver diseaseProinflammatory cytokine03 medical and health sciencesLiver diseaseMiceLiver Neoplasms ExperimentalmedicineAnimalsDiethylnitrosamineKinase activityTranscription Factor RelAGeneral Medicinemedicine.disease3. Good healthNeoplasm Proteins030104 developmental biologymedicine.anatomical_structureCell Transformation NeoplasticReceptors Tumor Necrosis Factor Type IHepatocyteReceptor-Interacting Protein Serine-Threonine KinasesCancer researchHepatocytesSignal TransductionResearch ArticleThe Journal of clinical investigation
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Interleukin-17A Promotes Lung Tumor Progression through Neutrophil Attraction to Tumor Sites and Mediating Resistance to PD-1 Blockade

2017

Abstract Introduction Proinflammatory cytokine interleukin-17A (IL-17A) is overexpressed in a subset of patients with lung cancer. We hypothesized that IL-17A promotes a protumorigenic inflammatory phenotype and inhibits antitumor immune responses. Methods We generated bitransgenic mice expressing a conditional IL-17A allele along with conditional Kras G12D and performed immune phenotyping of mouse lungs, a survival analysis, and treatment studies with antibodies either blocking programmed cell death 1 (PD-1) or IL-6 or depleting neutrophils. To support the preclinical findings, we analyzed human gene expression data sets and immune profiled patient lung tumors. Results Tumors in IL-17:Kras…

0301 basic medicinePulmonary and Respiratory MedicineChemokineLung NeoplasmsNeutrophilsLymphocytemedicine.medical_treatmentProgrammed Cell Death 1 ReceptorGene ExpressionMice TransgenicGranulocytemedicine.disease_causeArticleProinflammatory cytokineProto-Oncogene Proteins p21(ras)Mice03 medical and health sciencesImmune systemAnimalsHumansMedicineLung cancerbiologybusiness.industryInterleukin-17medicine.disease030104 developmental biologymedicine.anatomical_structureCytokineOncologyMutationImmunologyDisease Progressionbiology.proteinKRASbusinessJournal of Thoracic Oncology
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