Search results for "Host-Pathogen Interaction"

showing 10 items of 189 documents

Resveratrol-induced xenophagy promotes intracellular bacteria clearance in intestinal epithelial cells and macrophages

2019

International audience; Autophagy is a lysosomal degradation process that contributes to host immunity by eliminating invasive pathogens and the modulating inflammatory response. Several infectious and immune disorders are associated with autophagy defects, suggesting that stimulation of autophagy in these diseases should be bene ficial. Here, we show that resveratrol is able to boost xenophagy, a selective form of autophagy that target invasive bacteria. We demonstrated that resveratrol promotes in vitro autophagy-dependent clearance of intracellular bacteria in intestinal epithelial cells and macrophages. These results were validated in vivo using infection in a transgenic GFP-LC3 zebra f…

Salmonella typhimuriumrestrictionResveratrolresveratrolMicechemistry.chemical_compound0302 clinical medicine[SDV.IDA]Life Sciences [q-bio]/Food engineeringImmunologieXenophagyImmunology and AllergyIntestinal MucosaZebrafishOriginal Research0303 health sciencessalmonella infectionbiologyChemistrycrohns-disease[SDV.IDA] Life Sciences [q-bio]/Food engineering3. Good healthCell biologyrégime alimentaire030220 oncology & carcinogenesisHost-Pathogen InteractionsAIEClcsh:Immunologic diseases. AllergyautophagysalmonelleTransgenesalmonellaImmunologyautophagieCell Line03 medical and health sciencesImmune systemxenophagyEscherichia coliAnimalsHumans030304 developmental biologyselective autophagyhealthy-volunteersmodelEnterocolitisMacrophagesIntracellular parasiteAutophagylife-span extensionautophagy;resveratrol;xenophagy;salmonella;AIECagent resveratrolEpithelial Cellsbiology.organism_classification[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyCell cultureactivation[SDV.MP.BAC] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriologyproteinlcsh:RC581-607Bacteria
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Phylodynamic Analysis and Implication of HCV Genotype 4 Variability on Antiviral Drug Response and T-Cell Recognition.

2020

Therapies for HCV care could change the prevalence and the geographic distribution of genotypes due to differences in Sustained Virologic Response (SVR). In this scenario, uncommon genotypes/subtypes, such as genotype 4, could spread from high-risk groups, replacing genotypes eradicated by antiviral drugs. Genotype eradication is also strongly influenced by the CD8+ T cell response. In this study, the genetic variability in HCV genotype 4 strains obtained from a cohort of 67 patients na&iuml

Settore MED/07 - Microbiologia E Microbiologia ClinicaT-Lymphocyteslcsh:QR1-502Bayesian analysisHepacivirusViral Nonstructural Proteinslcsh:MicrobiologyCoalescent theoryphylodynamicGenotypegenetic variabilityPhylogenyBayesian analysimedia_commonSettore MED/12 - Gastroenterologiavirus diseasesMiddle Agedviral epitopeHepatitis CHost-Pathogen InteractionInfectious Diseasesmedicine.anatomical_structureHost-Pathogen InteractionsHCVtMRCADrugAdultGenotypemedicine.drug_classmedia_common.quotation_subjectT cellmacromolecular substancesHuman leukocyte antigenBiologyAntiviral AgentsArticleYoung AdultT cell recognitionVirologyDrug Resistance ViralmedicineHumansGenetic variabilitygenotype 4AgedDAAAntiviral AgentHepaciviruVirologydigestive system diseasesviral epitopesAntiviral drugCD8RASViruses
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AP-1 Transcription Factor Serves as a Molecular Switch between Chlamydia pneumoniae Replication and Persistence

2015

ABSTRACT Chlamydia pneumoniae is a Gram-negative bacterium that causes acute or chronic respiratory infections. As obligate intracellular pathogens, chlamydiae efficiently manipulate host cell processes to ensure their intracellular development. Here we focused on the interaction of chlamydiae with the host cell transcription factor activator protein 1 (AP-1) and its consequence on chlamydial development. During Chlamydia pneumoniae infection, the expression and activity of AP-1 family proteins c-Jun, c-Fos, and ATF-2 were regulated in a time- and dose-dependent manner. We observed that the c-Jun protein and its phosphorylation level significantly increased during C. pneumoniae development.…

Small interfering RNAGene knockdownCellular Microbiology: Pathogen-Host Cell Molecular InteractionsTranscription GeneticImmunologyChlamydiaeGene Expression Regulation BacterialHep G2 CellsChlamydophila pneumoniaeBiologybiology.organism_classificationMicrobiologyBacterial LoadMicrobiologyTranscription Factor AP-1AP-1 transcription factorInfectious DiseasesTranscription (biology)Host-Pathogen InteractionsHepatocytesHumansPhosphorylationParasitologyTranscription factorIntracellularInfection and Immunity
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Sympatric diversification vs. immigration: deciphering host-plant specialization in a polyphagous insect, the stolbur phytoplasma vector Hyalesthes o…

2012

The epidemiology of vector transmitted plant diseases is highly influenced by dispersal and the host-plant range of the vector. Widening the vector's host range may increase transmission potential, whereas specialization may induce specific disease cycles. The process leading to a vector's host shift and its epidemiological outcome is therefore embedded in the frameworks of sympatric evolution vs. immigration of preadapted populations. In this study, we analyse whether a host shift of the stolbur phytoplasma vector, Hyalesthes obsoletus from field bindweed to stinging nettle in its northern distribution range evolved sympatrically or by immigration. The exploitation of stinging nettle has l…

SympatryPhytoplasmaPopulationZoologyHemipteraGeneticsAnimalseducationEcology Evolution Behavior and SystematicsPhylogenyPlant Diseaseseducation.field_of_studyGenetic diversitybiologyEcologyHost (biology)Genetic VariationUrtica dioicaCixiidaebiology.organism_classificationBiological EvolutionSympatrySympatric speciationVector (epidemiology)Host-Pathogen InteractionsBiological dispersalMicrosatellite RepeatsMolecular ecology
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Intrahepatic myeloid-cell aggregates enable local proliferation of CD8+T cells and successful immunotherapy against chronic viral liver infection

2013

Chronic infection is difficult to overcome because of exhaustion or depletion of cytotoxic effector CD8(+) T cells (cytotoxic T lymphoytes (CTLs)). Here we report that signaling via Toll-like receptors (TLRs) induced intrahepatic aggregates of myeloid cells that enabled the population expansion of CTLs (iMATEs: 'intrahepatic myeloid-cell aggregates for T cell population expansion') without causing immunopathology. In the liver, CTL proliferation was restricted to iMATEs that were composed of inflammatory monocyte-derived CD11b(+) cells. Signaling via tumor-necrosis factor (TNF) caused iMATE formation that facilitated costimulation dependent on the receptor OX40 for expansion of the CTL popu…

T cellmedicine.medical_treatmentImmunologyPopulationGreen Fluorescent ProteinsMice TransgenicBiologyCD8-Positive T-LymphocytesLymphocytic ChoriomeningitisMicemedicineImmunology and AllergyCytotoxic T cellAnimalsLymphocytic choriomeningitis virusMyeloid CellseducationCell ProliferationMice Knockouteducation.field_of_studyLiver infectionCD11b AntigenMicroscopy ConfocalLiver DiseasesImmunotherapyReceptors OX40Flow CytometryMice Inbred C57BLCTL*Chronic infectionmedicine.anatomical_structureAnimals NewbornLiverToll-Like Receptor 9ImmunologyChronic DiseaseHost-Pathogen InteractionsImmunotherapyCD8Signal TransductionT-Lymphocytes CytotoxicNature Immunology
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Role of IFN-gamma in immune responses to Candida albicans infections

2014

Candida albicans is the most frequent etiologic agent that causes opportunistic fungal infections called candidiasis, a disease whose systemic manifestation could prove fatal and whose incidence is increasing as a result of an expanding immunocompromised population. Here we review the role of interferon-gamma (IFN-γ) in host protection against invasive candidiasis. This cytokine plays an essential role in both the innate and adaptive arms of the immune response to candidiasis. We focus on recent progress on host-pathogen interactions leading to the production of IFN-γ by host cells. IFN-γ is produced by CD4 Th1, CD8, γδ T, and natural killer (NK) cells, essentially in response to both IL-12…

T-LymphocytesFarmacologíamedicine.medical_treatmentPopulationReviewDiseaseMicrobiologyIFN-gammaInterferon-gammaImmune systemCandida albicansmedicineHumansInterferon gammaeducationCandida albicanseducation.field_of_studybiologyCandidiasisbiology.organism_classificationCorpus albicansKiller Cells NaturalCytokineImmune SystemHost-Pathogen InteractionsImmunologyTh17 CellsInfectionCD8medicine.drug
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From attachment to damage: defined genes of Candida albicans mediate adhesion, invasion and damage during interaction with oral epithelial cells.

2010

Candida albicans frequently causes superficial infections by invading and damaging epithelial cells, but may also cause systemic infections by penetrating through epithelial barriers. C. albicans is an unusual pathogen because it can invade epithelial cells via two distinct mechanisms: induced endocytosis, analogous to facultative intracellular enteropathogenic bacteria, and active penetration, similar to plant pathogenic fungi. Here we investigated the molecular basis of C. albicans epithelial interactions. By systematically assessing the contributions of defined fungal pathways and factors to different stages of epithelial interactions, we provide an expansive portrait of the processes an…

Transcription GeneticGenes Fungallcsh:MedicineMycologyPathogenesisEndocytosisMicrobiologyMicrobiologyFungal ProteinsCandidiasis OralStress PhysiologicalCandida albicansCell AdhesionHumansCell adhesionCandida albicanslcsh:SciencePathogenBiologyMicrobial PathogensFungal proteinMouthMultidisciplinarybiologyIntracellular parasitelcsh:RFungiFungal DiseasesGlyoxylatesEpithelial Cellsbiology.organism_classificationIsocitrate LyaseCorpus albicansUp-RegulationHost-Pathogen InteractionInfectious DiseasesCaco-2Medicinelcsh:QCaco-2 CellsTranscriptomeSuperficial MycosesResearch ArticlePLoS ONE
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The Transcription Factors TBX2 and TBX3 Interact with Human Papillomavirus 16 (HPV16) L2 and Repress the Long Control Region of HPVs

2013

ABSTRACT The minor capsid protein L2 of human papillomaviruses (HPVs) has multiple functions during the viral life cycle. Although L2 is required for effective invasion and morphogenesis, only a few cellular interaction partners are known so far. Using yeast two-hybrid screening, we identified the transcription factor TBX2 as a novel interaction partner of HPV type 16 (HPV16) L2. Coimmunoprecipitations and immunofluorescence analyses confirmed the L2-TBX2 interaction and revealed that L2 also interacts with TBX3, another member of the T-box family. Transcription of the early genes during HPV infection is under the control of an upstream enhancer and early promoter region, the long control r…

Transcription GeneticImmunologyBiologyCervical intraepithelial neoplasiaVirus ReplicationMicrobiologyViral life cycleTranscription (biology)VirologyTwo-Hybrid System TechniquesGene expressionProtein Interaction MappingmedicineHumansImmunoprecipitationGeneTranscription factorGeneticsHuman papillomavirus 16virus diseasesPromoterOncogene Proteins Viralmedicine.diseasefemale genital diseases and pregnancy complicationsGenome Replication and Regulation of Viral Gene ExpressionMicroscopy FluorescenceInsect ScienceHost-Pathogen InteractionsCapsid ProteinsT-Box Domain ProteinsChromatin immunoprecipitationHeLa Cells
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Paenibacillus larvae Chitin-Degrading Protein PlCBP49 Is a Key Virulence Factor in American Foulbrood of Honey Bees

2014

Paenibacillus larvae, the etiological agent of the globally occurring epizootic American Foulbrood (AFB) of honey bees, causes intestinal infections in honey bee larvae which develop into systemic infections inevitably leading to larval death. Massive brood mortality might eventually lead to collapse of the entire colony. Molecular mechanisms of host-microbe interactions in this system and of differences in virulence between P. larvae genotypes are poorly understood. Recently, it was demonstrated that the degradation of the peritrophic matrix lining the midgut epithelium is a key step in pathogenesis of P. larvae infections. Here, we present the isolation and identification of PlCBP49, a mo…

Veterinary MicrobiologyChitinPathogenesisPathology and Laboratory MedicineVirulence factorchemistry.chemical_compoundMedicine and Health SciencesPeritrophic matrixlcsh:QH301-705.5biologyVirulenceGram Positive BacteriaBeesVeterinary BacteriologyBacterial PathogensVeterinary DiseasesMedical MicrobiologyLarvaHost-Pathogen InteractionsPaenibacillusResearch Articlelcsh:Immunologic diseases. Allergy570American foulbroodVirulence FactorsImmunologyMolecular Sequence DataVirulenceMicrobiologyMicrobiologyChitinBacterial ProteinsVirologyGeneticsAnimalsAmino Acid SequenceMolecular BiologyMicrobial PathogensGram-Positive Bacterial InfectionsSequence Homology Amino AcidfungiBiology and Life SciencesMidgutBacteriologyHoney beebiology.organism_classificationlcsh:Biology (General)chemistryProteolysisParasitologyVeterinary Sciencelcsh:RC581-607BacteriaPLoS Pathogens
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Respiratory syncytial virus inhibits ciliagenesis in differentiated normal human bronchial epithelial cells: effectiveness of N-acetylcysteine.

2012

Persistent respiratory syncytial virus (RSV) infections have been associated with the exacerbation of chronic inflammatory diseases, including chronic obstructive pulmonary disease (COPD). This virus infects the respiratory epithelium, leading to chronic inflammation, and induces the release of mucins and the loss of cilia activity, two factors that determine mucus clearance and the increase in sputum volume. These alterations involve reactive oxygen species-dependent mechanisms. The antioxidant N-acetylcysteine (NAC) has proven useful in the management of COPD, reducing symptoms, exacerbations, and accelerated lung function decline. NAC inhibits RSV infection and mucin release in human A54…

Viral DiseasesPulmonologyChronic Obstructive Pulmonary Diseaseslcsh:MedicineMucin 5ACVirus ReplicationAcetylcysteinePulmonary Disease Chronic ObstructiveTubulinRespiratory systemlcsh:ScienceCells CulturedMultidisciplinaryInterleukin-13Microscopy VideoCell DifferentiationForkhead Transcription FactorsFree Radical Scavengersrespiratory systemHost-Pathogen InteractionLower Respiratory Tract InfectionsInfectious Diseasesmedicine.anatomical_structureInterleukin 13Medicinemedicine.symptomResearch Articlemedicine.drugDrugs and DevicesInflammationBronchiRespiratory Syncytial Virus InfectionsBiologyMicrobiologyAntiviral AgentsUpper Respiratory Tract InfectionsmedicineHumansCiliaBiologyInflammationRespiratory Syncytial Virus InfectionA549 cellMucinlcsh:RImmunityEpithelial CellsAxonemal DyneinsEpitheliumAcetylcysteineGene Expression RegulationRespiratory Syncytial Virus HumanRespiratory InfectionsImmunologyRespiratory epitheliumlcsh:QPLoS ONE
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