Search results for "INTERFERON"

showing 10 items of 963 documents

Visceral leishmaniasis during pegylated interferon therapy for chronic hepatitis C: first report.

2005

See: Puoti et al. Use of pegylated interferons is associated with an increased incidence of infections during combination treatment of chronic hepatitis C: a side effect of pegylation? Antiviral Therapy 2004; 9:627–630.

Pharmacologymedicine.medical_specialtySide effectbusiness.industryIncidence (epidemiology)medicine.diseaseVirologyGastroenterologyInfectious DiseasesCombined treatmentVisceral leishmaniasisChronic hepatitisPegylated interferonInternal medicinePEGylationMedicinePharmacology (medical)businessleishmaniasismedicine.drug
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Identificación de oportunidades de mejora del tratamiento de la hepatitis C

2006

® . Summary Objective: Hepatitis C represents a public health concern with more than 170 million carriers. The goal of this study was to identify improvement opportunities in the management of hepati- tis C, and the pharmaceutical actions performed for the preven- tion and solution of medication-related problems in patients seen at the Pharmaceutical Care Outpatient Unit.

Pharmacologymedicine.medical_specialtybusiness.industryPublic healthRibavirinMEDLINEAlpha interferonPeginterferon-alfaHepatitis Cmedicine.diseaseSurgerychemistry.chemical_compoundPharmaceutical carechemistryInternal medicinemedicineAdverse effectbusinessFarmacia Hospitalaria
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Antisense Phosphorothioate Oligonucleotides to the p65 Subunit of NF-κB Abrogate Fulminant Septic Shock Induced byS. typhimuriumin Mice

2001

The aim of this study was to characterize the functional relevance of the transcription factor NF-κB in the pathogenesis of septic shock. BALB/c mice were infected with two wild-type (WT 1, WT 2) strains of S. typhimurium that induce NF-κB or an escape variant that lacks this ability (P21) at a dose of 1 × 109/animal, respectively. Furthermore, wild-type infected mice were treated with antisense oligonucleotides directed against NF-κB 24 h before and 3 or 6 h after infection, while mismatched oligonucleotides were used as controls. Subsequently, the clinical course, histological and immunological alterations were monitored. Infection with WT 1 and WT 2 strains led to lethal septic shock wit…

Phosphorothioate OligonucleotidesNecrosisSeptic shockFulminantImmunologyInterleukinGeneral MedicineBiologymedicine.diseaseVirologyMolecular biologyPathogenesisInterferonmedicineTumor necrosis factor alphamedicine.symptommedicine.drugScandinavian Journal of Immunology
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The MAVS Immune Recognition Pathway in Viral Infection and Sepsis.

2021

Significance: It is estimated that close to 50 million cases of sepsis result in over 11 million annual fatalities worldwide. The pathognomonic feature of sepsis is a dysregulated inflammatory response arising from viral, bacterial, or fungal infections. Immune recognition of pathogen-associated molecular patterns is a hallmark of the host immune defense to combat microbes and to prevent the progression to sepsis. Mitochondrial antiviral signaling protein (MAVS) is a ubiquitous adaptor protein located at the outer mitochondrial membrane, which is activated by the cytosolic pattern recognition receptors, retinoic acid-inducible gene I (RIG-I) and melanoma differentiation associated gene 5 (M…

PhysiologyClinical BiochemistryBiologyBiochemistrySepsisImmune systemInterferonSepsismedicineAnimalsHumansMolecular BiologyGeneral Environmental ScienceMitochondrial antiviral-signaling proteinAdaptor Proteins Signal TransducingImmune EvasionLGP2Pattern recognition receptorSignal transducing adaptor proteinMDA5Cell Biologymedicine.diseaseForum Review ArticlesVirus DiseasesImmunologyHost-Pathogen InteractionsGeneral Earth and Planetary Sciencesmedicine.drugSignal TransductionAntioxidantsredox signaling
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Neutralization of interleukin-18 reduces severity in murine colitis and intestinal IFN-gamma and TNF-alpha production.

2001

Interleukin (IL)-18, initially described as interferon (IFN)-gamma-inducing factor, is expressed in the inflamed mucosa of patients with Crohn's disease. To investigate the role of IL-18 in intestinal inflammation, the effect of neutralizing antimurine IL-18 antiserum in dextran sulfate sodium (DSS)-induced colitis in BALB/c and C57BL/6 mice was examined. During a dose response of DSS, levels of colonic IL-18 increased parallel with clinical worsening. With the use of confocal laser microscopy, the increased IL-18 was localized to the intestinal epithelial layer. Anti-IL-18 treatment resulted in a dose-dependent reduction of the severity of colitis in both BALB/c and C57BL/6 mice. Colon sho…

PhysiologyColonmedicine.medical_treatmentInflammationIn Vitro TechniquesSeverity of Illness IndexInterferon-gammaMiceSpecies SpecificityInterferonPhysiology (medical)medicineAnimalsInterferon gammaColitisIntestinal MucosaMice Inbred BALB CDose-Response Relationship Drugbusiness.industryTumor Necrosis Factor-alphaImmune SeraDextran SulfateInterleukin-18Interleukinmedicine.diseaseColitisInterleukin-12digestive system diseasesMice Inbred C57BLDisease Models AnimalCytokineImmunologyInterleukin 12Leukocytes MononuclearInterleukin 18Femalemedicine.symptombusinessInjections Intraperitonealmedicine.drugAmerican journal of physiology. Regulatory, integrative and comparative physiology
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TLR4 abrogates the Th1 immune response through IRF1 and IFN-β to prevent immunopathology during L. infantum infection

2020

A striking feature of human visceral leishmaniasis (VL) is chronic inflammation in the spleen and liver, and VL patients present increased production levels of multiple inflammatory mediators, which contribute to tissue damage and disease severity. Here, we combined an experimental model with the transcriptional profile of human VL to demonstrate that the TLR4-IFN-β pathway regulates the chronic inflammatory process and is associated with the asymptomatic form of the disease. Tlr4-deficient mice harbored fewer parasites in their spleen and liver than wild-type mice. TLR4 deficiency enhanced the Th1 immune response against the parasite, which was correlated with an increased activation of de…

PhysiologyGene ExpressionWhite Blood CellsMiceCell SignalingAnimal CellsImmune PhysiologyZoonosesImmunopathologyMedicine and Health SciencesMembrane Receptor SignalingBiology (General)Immune ResponseLeishmaniasisProtozoansLeishmaniaMice Knockout0303 health sciencesbiologyT Cells030302 biochemistry & molecular biologyEukaryotaImmune Receptor SignalingInfectious Diseasesmedicine.anatomical_structureLeishmaniasis VisceralCellular Typesmedicine.symptomLeishmania infantumResearch ArticleSignal TransductionNeglected Tropical DiseasesQH301-705.5Leishmania InfantumImmune CellsImmunologySpleenInflammationLEISHMANIOSE VISCERALMicrobiology03 medical and health sciencesImmune systemVirologyParasitic DiseasesGeneticsmedicineAnimalsMolecular Biology030304 developmental biologyInflammationProtozoan InfectionsBlood CellsOrganismsBiology and Life SciencesCell BiologyInterferon-betaTh1 CellsRC581-607Tropical Diseasesmedicine.diseasebiology.organism_classificationParasitic ProtozoansToll-Like Receptor 4IRF1Visceral leishmaniasisImmunologyTLR4ParasitologyImmunologic diseases. AllergySpleenInterferon Regulatory Factor-1
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Enhanced in vivo targeting of murine nonparenchymal liver cells with monophosphoryl lipid A functionalized microcapsules.

2014

A broad spectrum of infectious liver diseases emphasizes the need of microparticles for targeted delivery of immunomodulatory substances to the liver. Microcapsules (MCs) are particularly attractive for innovative drug and vaccine formulations, enabling the combination of antigen, drugs, and adjuvants. The present study aimed to develop microcapsules characterized by an enhanced liver deposition and accelerated uptake by nonparenchymal liver cells (NPCs). Initially, two formulations of biodegradable microcapsules were synthesized from either hydroxyethyl starch (HES) or mannose. Notably, HES-MCs accumulated primarily in the liver, while mannose particles displayed a lung preference. Functio…

Polymers and PlasticsLiver cytologyKupffer CellsMonophosphoryl Lipid AMannoseBioengineeringCapsulesReceptors Cell SurfacePharmacologyBiomaterialsMinor Histocompatibility Antigenschemistry.chemical_compoundInterferon-gammaMiceImmune systemDrug Delivery SystemsAntigenPhagocytosisIn vivoAntigens CDMaterials ChemistryAnimalsSecretionLectins C-TypeCD40 AntigensInterleukin-6Tumor Necrosis Factor-alphaLiver DiseasesDendritic CellsIn vitroMice Inbred C57BLToll-Like Receptor 4Lipid AchemistryBiochemistryLiverNanoparticlesFemaleBiomacromolecules
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Cytokines and growth factors in wound drainage fluid from patients undergoing incisional hernia repair.

2006

Knowing the dynamics of growth factor and cytokine secretion within the site of a surgical operation is important, as they play a crucial role in the pathophysiology of wound healing and are a target for modifying the repair response. The aim of this study was to evaluate the production of several cytokines and growth factors in the drainage wound fluid from patients undergoing incisional hernia repair: namely, interleukin (IL)-6, IL-10, IL-1alpha, IL-1 ra, interferon-gamma, vascular endothelial growth factors and basic fibroblast growth factor. Ten female patients with abdominal midline incisional hernia undergoing surgical repair were included in this study. In all cases, a closed-suction…

Postoperative CareVascular Endothelial Growth Factor AGRANULATION-TISSUE FORMATIONInterleukinsSKIN FLAPSPROFILESExudates and TransudatesMiddle AgedSuctionVEGFHernia VentralFACTOR EXPRESSIONEARLY SURGICAL WOUNDSInterferon-gammaCOLORECTAL SURGERYSURVIVALMEDIATES ANGIOGENIC ACTIVITYCytokinesHumansFemaleFibroblast Growth Factor 2Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society
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Acute organ failure following the loss of anti-apoptotic cellular FLICE-inhibitory protein involves activation of innate immune receptors

2014

Apoptosis signaling is involved in both physiological tissue homeostasis and acute and chronic diseases. The role of regulatory apoptosis signaling molecules and their organ-specific functions are less defined. Therefore, we investigated the loss of the anti-apoptotic cellular FLICE-inhibitory protein (cFLIP) and the mechanisms of the resulting lethal organ failure in vivo using inducible knockout mice. These were generated by crossing floxed cFLIP mice to a tamoxifen inducible Rosa26-creERT2 mouse strain. Death following global loss of cFLIP resulted from liver failure, accumulation of M1-polarized macrophages and accompanying hepatic cell death and inflammation. Apoptosis was also promine…

Programmed cell deathCASP8 and FADD-Like Apoptosis Regulating ProteinMice TransgenicInflammationBiologyMiceImmune systemmedicineAnimalsMolecular BiologyTissue homeostasisOriginal PaperInnate immune systemMacrophagesMembrane ProteinsCell BiologyLiver Failure AcuteImmunity InnateCell biologyToll-Like Receptor 4TransplantationApoptosisToll-Like Receptor 9Stimulator of interferon genesHepatocytesmedicine.symptomCell Death & Differentiation
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Met inhibition revokes IFNγ-induction of PD-1 ligands in MET-amplified tumours

2019

BACKGROUND: Interferon-induced expression of programmed cell death ligands (PD-L1/PD-L2) may sustain tumour immuneevasion. Patients featuring MET amplification, a genetic lesion driving transformation, may benefit from anti-MET treatment. We explored if MET-targeted therapy interferes with Interferon-gamma modulation of PD-L1/PD-L2 in MET-amplified tumours.METHODS: PD-L1/PD-L2 expression and signalling pathways downstream of MET or Interferon-gamma were analysed in MET-amplified tumour cell lines and in patient-derived tumour organoids, in basal condition, upon Interferon-gamma stimulation, and after anti-MET therapy.RESULTS: PD-L1 and PD-L2 were upregulated in MET-amplified tumour cells up…

Programmed cell deathCancer ResearchCancer immunotherapyMET-amplified tumoursB7-H1 AntigenArticleInterferon-gammaTargeted therapiesDownregulation and upregulationInterferonCell Line TumorNeoplasmsHumansMedicineMet inhibitionMolecular Targeted TherapySTAT1Kinase activityReceptorProtein Kinase InhibitorsJanus KinasesReceptors InterferonOncogenebiologyPD-1 ligandsbusiness.industryLiver NeoplasmsOncogenesProto-Oncogene Proteins c-metProgrammed Cell Death 1 Ligand 2 ProteinOrganoidsSTAT1 Transcription FactorOncologybiology.proteinCancer researchOncology; Cancer Research; Met inhibition; IFNγ-induction;PD-1 ligands; MET-amplified tumoursTumor EscapeSignal transductionColorectal NeoplasmsbusinessIFNγ-inductionSignal Transductionmedicine.drug
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