Search results for "Pathogenesis"

showing 10 items of 761 documents

Role of serum interleukin-6 in deciding therapy for multidrug resistant oral lichen planus

2015

Background: Oral lichen planus (OLP) is a T cell mediated immune response. T cells locally present in the involved tissues release cytokines like interleukin-6 (IL-6), which contributes to pathogenesis of OLP. Also IL-6 has been associated with multidrug resistance protein (MRP) expression by keratinocytes. Correspondingly, upregulation of MRP was found in OLP. We conducted this study to evaluate the effects of various drugs on serum IL-6 in OLP; and correlation of these effects with the nature of clinical response and resistance pattern seen in OLP lesions with various therapeutic modalities. Thus we evaluated the role of serum IL-6 in deciding therapy for multidrug resistant OLP. Material…

T cellOdontologíaPathogenesisPimecrolimusImmune systemstomatognathic systemMedicineInterleukin 6General DentistryOral Medicine and Pathologybiologybusiness.industryResearchmedicine.disease:CIENCIAS MÉDICAS [UNESCO]Ciencias de la saludstomatognathic diseasesmedicine.anatomical_structureImmunologyUNESCO::CIENCIAS MÉDICASbiology.proteinBiomarker (medicine)MethotrexateOral lichen planusbusinessmedicine.drugJournal of Clinical and Experimental Dentistry
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Activation of complement by the alternative pathway as a factor in the pathogenesis of periodontal disease.

1976

Dental plaque and a bacterium, Actinomyces viscosus, isolated from plaque that can reproduce periodontal disease in germ-free rats, are activators of complement by the alternative pathway. It is suggested that this process is involved in the pathogenesis of chronic inflammatory periodontal disease.

T-LymphocytesGuinea PigsDental PlaqueAntigen-Antibody ComplexDental plaquePathogenesisstomatognathic systemPeriodontal diseasemedicineActinomycesAnimalsHumansActinomyces viscosusBone ResorptionPeriodontitisGlycoproteinsB-LymphocytesEnzyme Precursorsbusiness.industryMacrophagesGlobulinsGeneral MedicineComplement C3Complement System Proteinsmedicine.diseaseCathepsinsComplement (complexity)RatsEndotoxinsstomatognathic diseasesMicrobial CollagenaseImmunologyAlternative complement pathwaybusinessLancet (London, England)
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Cutting Edge: IL-23 Cross-Regulates IL-12 Production in T Cell-Dependent Experimental Colitis

2006

Abstract Although IL-12 and IL-23 share the common p40 subunit, IL-23, rather than IL-12, seems to drive the pathogenesis of experimental autoimmune encephalomyelitis and arthritis, because IL-23/p19 knockout mice are protected from disease. In contrast, we describe in this study that newly created LacZ knockin mice deficient for IL-23 p19 were highly susceptible for the development of experimental T cell-mediated TNBS colitis and showed even more severe colitis than wild-type mice by endoscopic and histologic criteria. Subsequent studies revealed that dendritic cells from p19-deficient mice produce elevated levels of IL-12, and that IL-23 down-regulates IL-12 expression upon TLR ligation. …

T-LymphocytesTransgeneT cellImmunologyDown-RegulationMice TransgenicInterleukin-23PathogenesisMiceInterleukin 23AnimalsImmunology and AllergyMedicineColitisCells Culturedbusiness.industryInterleukinsExperimental autoimmune encephalomyelitisColitismedicine.diseaseInterleukin-12Survival RateDisease Models AnimalProtein Subunitsmedicine.anatomical_structureImmunologyKnockout mouseInterleukin-23 Subunit p19Interleukin 12Disease SusceptibilitybusinessThe Journal of Immunology
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Lights and shadows of the Taenia asiatica life cycle and pathogenicity.

2013

Humans are definitive hosts of two well-known species of the Taenia genus, Taenia solium (the pig tapeworm) and Taenia saginata (the cattle tapeworm). In the 1990s, a third species, Taenia asiatica, was discovered, sharing features with the other two since the adult morphology is similar to that of T. saginata, but its life cycle is like that of T. solium. Human taeniasis usually is asymptomatic or displays mild symptoms, and only T. solium can cause other sometimes serious disorders when humans accidentally ingest the eggs and develop the larval stage in different organs (cysticercosis). In this review, we expose what we currently know (lights) and what we do not yet know (shadows) about t…

Taenia asiaticaPathologymedicine.medical_specialtySymposiumbiologyHuman liverLife cyclepathogenesisZoologyCysticercosisbiology.organism_classificationmedicine.diseasePathogenicityTaenia asiaticamedicine.drug_formulation_ingredientTaenia soliumparasitic diseasesmedicineTaeniaTaeniasisTropismTropical parasitology
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Extracellular vesicles in airway homeostasis and pathophysiology

2021

The epithelial–mesenchymal trophic unit (EMTU) is a morphofunctional entity involved in the maintenance of the homeostasis of airways as well as in the pathogenesis of several diseases, including asthma and chronic obstructive pulmonary disease (COPD). The “muco-microbiotic layer” (MML) is the innermost layer of airways made by microbiota elements (bacteria, viruses, archaea and fungi) and the surrounding mucous matrix. The MML homeostasis is also crucial for maintaining the healthy status of organs and its alteration is at the basis of airway disorders. Nanovesicles produced by EMTU and MML elements are probably the most important tool of communication among the different cell types, inclu…

TechnologyCell typenanovesiclesQH301-705.5QC1-999Asthma Chronic obstructive pulmonary diseaseCOPDEpithelial–mesenchymal trophic unitExosomesMicrobiota Muco-microbiotic layer nanovesicles Outer membrane vesicles.Biologychronic obstructive pulmonary diseasePathogenesismedicineCOPDGeneral Materials ScienceBiology (General)QD1-999InstrumentationAsthmaFluid Flow and Transfer ProcessesCOPDSettore BIO/16 - Anatomia UmanaTPhysicsProcess Chemistry and TechnologyGeneral EngineeringasthmaEngineering (General). Civil engineering (General)medicine.diseasemuco-microbiotic layerMicrovesiclesPathophysiologyrespiratory tract diseasesComputer Science ApplicationsChemistryepithelial–mesenchymal trophic unitImmunologyTA1-2040AirwayHomeostasis
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Anti-fetal immune response mechanisms may be involved in the pathogenesis of placental abruption

2003

Placental abruption is an unpredictable severe complication in pregnancy. In order to investigate the possibility that the activation of the fetal nonadaptive immune system may be involved in the pathogenesis of this disease, IL-6 release from cord blood monocytes was examined by intracellular cytokine staining and flow cytometric analysis. Our results demonstrate that preterm placental abruption (n = 15) in contrast to uncontrollable preterm labor (n = 33) is associated with significantly (P < 0.001) increased release of IL-6 from the fetal monocytes. The same holds true for rhesus disease (n = 9, P < 0.001) that is characterized by a maternal production of antibodies against the rhesus-D …

Time FactorsImmunologyAntibodiesMonocytesPreeclampsiaPathogenesisFetusObstetric Labor PrematureImmune systemHLA AntigensPregnancyHumansImmunology and AllergyMedicineAbruptio PlacentaeFetusPregnancybiologyPlacental abruptionbusiness.industryImmunityFetal Bloodmedicine.diseaseFetal circulationImmunologybiology.proteinFemaleAntibodybusinessClinical Immunology
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The aryl hydrocarbon receptor modulates acute and late mast cell responses.

2012

Abstract The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor whose activity is modulated by xenobiotics as well as physiological ligands. These compounds may modulate inflammatory responses and contribute to the rising prevalence of allergic diseases observed in industrialized countries. Mast cells (MCs), located within tissues at the boundary of the external environment, represent a potential target of AhR ligands. In this study, we report that murine and human MCs constitutively express AhR, and its activation by the high-affinity ligand 6-formylindolo[3,2-b]carbazole (FICZ) determines a boost in degranulation. On the contrary, repeated exposure to FICZ inhibits…

Time FactorsInbred C57BLLigandsCell DegranulationPathogenesischemistry.chemical_compoundMiceAnaphylaxiReceptorsMast CellImmunology and AllergyMast CellsReceptorMice KnockoutbiologyInterleukin-17DegranulationMast cellUp-RegulationImmunology Mast Cell Aryl Receptormedicine.anatomical_structureAryl HydrocarbonBone Marrow Celldeficiency/metabolism/physiologyIgEmedicine.symptomimmunology/metabolism/pathologyHistamineHumanReceptorTime FactorKnockoutImmunologyDown-RegulationLigandInflammationBone Marrow CellsSettore MED/08 - Anatomia PatologicaCell LinebiosynthesiAnaphylaxis; immunology/metabolism/pathology Animals Bone Marrow Cells; immunology/metabolism/pathology Cell Degranulation; genetics/immunology Cell Line Down-Regulation; genetics/immunology Humans Interleukin-17; biosynthesis Interleukin-6; biosynthesis Ligands Mast Cells; immunology/metabolism/pathology Mice Mice; Inbred C57BL Mice; Knockout Receptors; Aryl Hydrocarbon; deficiency/metabolism/physiology Receptors; IgE; physiology Time Factors Up-Regulation; genetics/immunologymedicineAnimalsHumansTranscription factorAnaphylaxisAnimalInterleukin-6Receptors IgEAryl hydrocarbon receptorgenetics/immunologyMice Inbred C57BLMAST CELL; ARYL HYDROCARBON RECEPTORchemistryReceptors Aryl HydrocarbonImmunologyphysiologybiology.proteinbiosynthesisJournal of immunology (Baltimore, Md. : 1950)
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Role of tir and intimin in the virulence of rabbit enteropathogenic Escherichia coli serotype O103:H2.

2000

ABSTRACT Attaching and effacing (A/E) rabbit enteropathogenic Escherichia coli (REPEC) strains belonging to serogroup O103 are an important cause of diarrhea in weaned rabbits. Like human EPEC strains, they possess the locus of enterocyte effacement clustering the genes involved in the formation of the A/E lesions. In addition, pathogenic REPEC O103 strains produce an Esp-dependent but Eae (intimin)-independent alteration of the host cell cytoskeleton characterized by the formation of focal adhesion complexes and the reorganization of the actin cytoskeleton into bundles of stress fibers. To investigate the role of intimin and its translocated coreceptor (Tir) in the pathogenicity of REPEC, …

Time Factors[SDV]Life Sciences [q-bio]MutantAdministration OralPATHOGENICITEmedicine.disease_causeBacterial AdhesionMICROSCOPIE ELECTRONIQUE A TRANSMISSIONFecesCytoskeleton0303 health sciencesVirulenceEscherichia coli ProteinsEnterobacteriaceae3. Good health[SDV] Life Sciences [q-bio]IntestinesInfectious DiseasesMolecular and Cellular PathogenesisRabbitsLocus of enterocyte effacementBacterial Outer Membrane ProteinsImmunologyMolecular Sequence DataVirulenceReceptors Cell SurfaceBiologyMicrobiologydigestive systemMicrobiologyCell Line03 medical and health sciencesBacterial ProteinsIleummedicineEscherichia coliAnimalsHumansEnteropathogenic Escherichia coliAdhesins BacterialEscherichia coli030304 developmental biologyIntiminModels Genetic030306 microbiologyGenetic Complementation TestEpithelial Cellsbiochemical phenomena metabolism and nutritionbiology.organism_classificationActin cytoskeleton[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyActinsKineticsMicroscopy ElectronMicroscopy FluorescenceMutagenesisParasitologyCarrier ProteinsHeLa CellsInfection and immunity
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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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Immune Evasion Proteins Enhance Cytomegalovirus Latency in the Lungs

2009

ABSTRACT CD8 T cells control cytomegalovirus (CMV) infection in bone marrow transplantation recipients and persist in latently infected lungs as effector memory cells for continuous sensing of reactivated viral gene expression. Here we have addressed the question of whether viral immunoevasins, glycoproteins that specifically interfere with antigen presentation to CD8 T cells, have an impact on viral latency in the murine model. The data show that deletion of immunoevasin genes in murine CMV accelerates the clearance of productive infection during hematopoietic reconstitution and leads to a reduced latent viral genome load, reduced latency-associated viral transcription, and a lower inciden…

Transcription GeneticImmunologyAntigen presentationAntigen-Presenting CellsCytomegalovirusBone Marrow CellsGenome ViralCD8-Positive T-LymphocytesBiologymedicine.disease_causeMicrobiologyHerpesviridaeVirusMiceImmune systemRecurrenceVirologyVirus latencymedicineAnimalsCytotoxic T cellAntigen-presenting cellLungGlycoproteinsMice Inbred BALB Cmedicine.diseaseVirologyVirus LatencyInsect ScienceCytomegalovirus InfectionsImmunologyPathogenesis and ImmunityFemaleViral diseaseJournal of Virology
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