Search results for "host defense"

showing 6 items of 6 documents

Innate immune response to tick-borne pathogens: Cellular and molecular mechanisms induced in the hosts

2020

This article belongs to the Special Issue Inflammasome.

0301 basic medicineInnate immune responseHost Defense MechanismReviewInflammasomelcsh:ChemistryTicksTheileriaTick borne pathogensRickettsialcsh:QH301-705.5SpectroscopyGene ontology analysisgene ontology analysisInflammasomeGeneral MedicineAcquired immune systemComputer Science ApplicationsTick-Borne DiseasesTumor necrosis factor alphamedicine.drugAnaplasma030106 microbiologyEhrlichiaBabesiaBiologyCatalysisMicrobiologyInorganic Chemistry03 medical and health sciencesAntigeninflammasomeparasitic diseasesmedicineAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyInnate immune systemOrganic Chemistrygene ontology analysibiology.organism_classificationImmunity InnateComplement systemInsect Vectors030104 developmental biologyRickettsialcsh:Biology (General)lcsh:QD1-999innate immune responsetick borne pathogens
researchProduct

Plasma granulysin levels and cellular interferon-gamma production correlate with curative host responses in tuberculosis, while plasma interferon-gam…

2007

Contains fulltext : 52707.pdf (Publisher’s version ) (Closed access) Granulysin is a recently identified cytolytic protein which is expressed by human cytotoxic T-lymphocytes and natural killer (NK)-cells, and has broad antimicrobial and tumoricidal activity. Circulating granulysin levels are associated with T- and NK-cell activity, and may thus reflect protection-associated cellular immune responses. In a case-control study in Indonesia, a highly tuberculosis (TB)-endemic country, we therefore determined plasma granulysin levels in adults with active pulmonary TB before, during, and after TB treatment, both in mild/moderate-TB and advanced-TB patients, and compared these to healthy neighbo…

AdultAntigens Differentiation T-LymphocyteMaleMicrobiology (medical)TuberculosisAdolescentInfectious diseases and international health [NCEBP 13]TuberculosiImmunologyEnzyme-Linked Immunosorbent AssayBiologySeverity of Illness IndexMicrobiologyInterferon-gammaImmune systemAntigenImmunitymedicineHumansCytotoxic T cellInterferon gammaPlasma granulysinCellular granulysinCellular IFN-gGranulysinDisease severityTuberculosis PulmonaryAgedImmunity CellularInterferon-gamma productionPoverty-related infectious diseases [N4i 3]Immunotherapy gene therapy and transplantation [UMCN 1.4]Middle Agedmedicine.diseasePathogenesis and modulation of inflammation [N4i 1]Infectious DiseasesCase-Control StudiesPlasma IFN-gImmunologyFemaleMicrobial pathogenesis and host defense [UMCN 4.1]medicine.drugImmunity infection and tissue repair [NCMLS 1]
researchProduct

Glycogen synthase 2 is a novel target gene of peroxisome proliferator-activated receptors.

2007

International audience; Glycogen synthase 2 (Gys-2) is the ratelimiting enzyme in the storage of glycogen in liver and adipose tissue, yet little is known about regulation of Gys-2 transcription. The peroxisome proliferator-activated receptors (PPARs) are transcription factors involved in the regulation of lipid and glucose metabolism and might be hypothesized to govern glycogen synthesis as well. Here, we show that Gys-2 is a direct target gene of PPARalpha, PPARbeta/delta and PPARgamma. Expression of Gys-2 is significantly reduced in adipose tissue of PPARalpha-/-, PPARbeta/delta-/- and PPARgamma+/- mice. Furthermore, synthetic PPARbeta/delta, and gamma agonists markedly up-regulate Gys-2…

Animals; Chromatin/ultrastructure; DNA Primers; Gene Expression Regulation Enzymologic; Glycogen Synthase/genetics; Hepatocytes/enzymology; Hepatocytes/physiology; Mice; Mice Knockout; Peroxisome Proliferator-Activated Receptors/deficiency; Peroxisome Proliferator-Activated Receptors/genetics; Polymerase Chain Reaction; RNA/genetics; RNA/isolation & purification; Rats; Transcription GeneticTranscription GeneticPeroxisome proliferator-activated receptorMESH : HepatocytesPPREPolymerase Chain Reactionadipose-tissuePPARMESH: HepatocytesMice0302 clinical medicineMESH: Animals610 Medicine & healthchemistry.chemical_classificationRegulation of gene expression0303 health sciencesGlycogenglycogen-synthaseChromatinGlycogen Synthase030220 oncology & carcinogenesisMESH : DNA PrimersmicroarrayMESH: DNA Primersmedicine.medical_specialtyHealth aging / healthy living [IGMD 5]fatty-acid oxidationliverGene Expression Regulation EnzymologicMESH: Chromatin03 medical and health sciencesskeletal-muscleGlycogen synthaseMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyHNF4αVLAGPharmacologybeta/deltaMESH: Polymerase Chain Reactionresponse elementsMESH : Peroxisome Proliferator-Activated ReceptorsEndocrinologychemistryMicrobial pathogenesis and host defense [UMCN 4.1]Response elementPeroxisome Proliferator-Activated ReceptorsAdipose tissueMESH: Peroxisome Proliferator-Activated Receptorsin-vivoMESH: Mice KnockoutTransactivationchemistry.chemical_compoundVoeding Metabolisme en GenomicaMESH : RNAMESH : Polymerase Chain ReactionMice KnockoutMESH : ChromatinMESH : RatsMESH: Gene Expression Regulation EnzymologicMetabolism and Genomicsadipose tissueMetabolisme en GenomicaMolecular MedicineNutrition Metabolism and GenomicsMESH : Glycogen SynthaseResearch ArticleMESH: Ratsglycogen synthase 2610 Medicine & healthBiologyMESH : Gene Expression Regulation EnzymologicCellular and Molecular NeuroscienceVoedingMESH: RNAInternal medicineMESH : MicemedicineAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyTranscription factorMESH: Micealpha ppar-alpha030304 developmental biologyNutritionDNA PrimersMESH: Glycogen SynthaseMESH: Transcription GeneticMESH : Transcription GeneticCell BiologyRatsgene transcriptionbiology.proteinHepatocytesRNAMESH : Mice KnockoutgammaMESH : Animalsmetabolism
researchProduct

Complement Activation during Critical Illness: Current Findings and an Outlook in the Era of COVID-19

2020

Rationale: Complement is crucial for host defense but may also drive dysregulated inflammation. There is limited understanding of alternative complement function, which can amplify all complement activity, during critical illness. Objectives: We examined the function and key components of the alternative complement pathway in a series of critically ill patients and in a mouse pneumonia model. Methods: Total classical (CH50) and alternative complement (AH50) function were quantified in serum from 321 prospectively enrolled critically ill patients and compared with clinical outcomes. Alternative pathway (AP) regulatory factors were quantified by ELISA (n = 181) and examined via transcriptomic…

MalePulmonary and Respiratory Medicine2019-20 coronavirus outbreakPsychotherapistCritical CareCoronavirus disease 2019 (COVID-19)Critical IllnessSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2)Complement Pathway AlternativePneumonia ViralCritical Care and Intensive Care MedicineMiceBetacoronavirusAnimalsHumanspneumoniaMedicinecomplementPandemicsAgedRetrospective StudiesSARS-CoV-2business.industryEditorialsCOVID-19Original ArticlesMiddle AgedPennsylvaniaSurvival AnalysisComplement systemhost defenseCritical illnessFemaleCoronavirus InfectionsbusinessserumCoronavirus InfectionsAmerican Journal of Respiratory and Critical Care Medicine
researchProduct

New active drugs against liver stages of Plasmodium predicted by molecular topology.

2008

ABSTRACT We conducted a quantitative structure-activity relationship (QSAR) study based on a database of 127 compounds previously tested against the liver stage of Plasmodium yoelii in order to develop a model capable of predicting the in vitro antimalarial activities of new compounds. Topological indices were used as structural descriptors, and their relation to antimalarial activity was determined by using linear discriminant analysis. A topological model consisting of two discriminant functions was created. The first function discriminated between active and inactive compounds, and the second identified the most active among the active compounds. The model was then applied sequentially t…

Quantitative structure–activity relationshipStereochemistryAntiparasiticmedicine.drug_classModels BiologicalAuto-immunity transplantation and immunotherapy [N4i 4]AntimalarialsMiceStructure-Activity RelationshipParasitic Sensitivity Testsparasitic diseasesmedicineAnimalsHumansStructure–activity relationshipPharmacology (medical)PharmacologybiologyPoverty-related infectious diseases [N4i 3]Plasmodium falciparumPlasmodium yoeliibiology.organism_classificationIn vitroInfectious Diseasesmedicine.anatomical_structureLiverBiochemistrySusceptibilityHepatocyteHepatocytesMicrobial pathogenesis and host defense [UMCN 4.1]Infection and autoimmunity [NCMLS 1]Plasmodium yoeliiFunction (biology)Immunity infection and tissue repair [NCMLS 1]
researchProduct

Treatment with a CO-releasing molecule (CORM-3) reduces joint inflammation and erosion in murine collagen-induced arthritis.

2008

Contains fulltext : 70589.pdf (Publisher’s version ) (Closed access) OBJECTIVE: CO-releasing molecules (CO-RMs) are a novel class of anti-inflammatory agents. We have examined the possible therapeutic effects of CORM-3 in collagen-induced arthritis (CIA). METHODS: Arthritis was induced in DBA-1/J mice by type II collagen. Animals were treated with CORM-3 (5 and 10 mg/kg/day, intraperitoneally) or the inactive compound iCORM-3 (10 mg/kg/day, intraperitoneally) unable to release CO, from days 22 to 31. Production of anti-type II collagen antibodies, cytokines and cartilage olimeric matrix protein (COMP) was evaluated by enzyme-linked immunosorbent assay, and prostaglandin E(2) (PGE(2)) by rad…

musculoskeletal diseasesmedicine.medical_treatmentImmunologyAnti-Inflammatory AgentsDrug Evaluation PreclinicalType II collagenArthritisInflammationPharmacologyAuto-immunity transplantation and immunotherapy [N4i 4]DinoprostoneGeneral Biochemistry Genetics and Molecular BiologyMiceRheumatologyOrganometallic CompoundsPerception and Action [DCN 1]medicineAnimalsImmunology and AllergyChronic inflammation and autoimmunity [UMCN 4.2]Dose-Response Relationship Drugbiologybusiness.industryRANK LigandInterleukinIntercellular Adhesion Molecule-1medicine.diseaseArthritis ExperimentalPathogenesis and modulation of inflammation [N4i 1]Cellular infiltrationCyclooxygenase 2Mice Inbred DBARANKLImmunologybiology.proteinCytokinesTumor necrosis factor alphaMicrobial pathogenesis and host defense [UMCN 4.1]Inflammation Mediatorsmedicine.symptombusinessInfection and autoimmunity [NCMLS 1]Heme Oxygenase-1Immunity infection and tissue repair [NCMLS 1]Prostaglandin E
researchProduct