Search results for "pathogenesi"

showing 10 items of 764 documents

Mucosal immunoregulation: transcription factors as possible therapeutic targets.

2005

Much progress has been recently made with regard to our understanding of the mucosal immune system in health and disease. In particular, it has been shown that uncontrolled mucosal immune responses driven by lymphocytes or non-lymphoid cells may lead to immunological diseases such as allergy, hypersensitivity and inflammation. Thus, a more detailed understanding of mucosal immune regulation and decision making at mucosal surfaces is essential for a better understanding of mucosal immune responses in health and disease. Antigen presenting cells and T lymphocytes play a key role in controlling mucosal immune responses. To deal with this key task, T helper cells differentiate into functionally…

AllergyImmunologyInflammationApoptosisSuppressor of Cytokine Signaling ProteinsAllergic inflammationPathogenesisImmune systemImmunitymedicineHypersensitivityImmunology and AllergyAnimalsHumansIL-2 receptorMast CellsAntigen-presenting cellGlucocorticoidsImmunity MucosalPharmacologybusiness.industrymedicine.diseaseInflammatory Bowel DiseasesAsthmaIntestinesSuppressor of Cytokine Signaling 3 ProteinImmunologyCytokinesmedicine.symptombusinessTranscription FactorsCurrent drug targets. Inflammation and allergy
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Human asialoglycoprotein receptor as an autoantigen in chronic hepatitis.

1991

ASGPR may play a role in the pathogenesis of autoimmune chronic liver diseases. Several lines of evidence support this hypothesis. Antibodies to rabbit ASGPR could be found in various inflammatory liver diseases. In contrast, ASGPR preparations derived from human liver (h-ASGPR) were recognized predominantly by sera from patients with ai-CAH. Moreover, anti-h-ASGPR showed a close correlation to the inflammatory activity of ai-CAH both in terms of prevalence (88% in histologically proven active diseases), immunoglobulin class (IgM antibodies restricted to active inflammation) and behavior during treatment. Anti-h-ASGPR secretion could also be found in vitro, when PBL of patients were stimula…

AllergyT-LymphocytesImmunologyDiseaseAsialoglycoprotein ReceptorAutoantigensPathogenesisPrimary biliary cirrhosismedicineAnimalsHumansReceptors ImmunologicAutoantibodiesHepatitis ChronicImmunity Cellularbiologybusiness.industryAutoantibodymedicine.diseaseLiverPeripheral blood lymphocyteImmunologybiology.proteinAsialoglycoprotein receptorAntibodybusinessImmunosuppressive AgentsImmunologic research
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Acquired and Hereditary Angioedema: Pathogenesis and Therapy

1988

There are two main pathogenetic ways by which angioedema can develop. These pathways are completely different and lead to completely different diseases, which may have angioedema of the skin in common. Most cases of cutaneous angioedema develop with involvement of the mast cell and its mediators; especially histamine is considered to play a major role. The exact pathogenesis, however, is not known. This type of angioedema is assumed to be related to urticaria for several reasons: 1 Often it appears alternately with urticaria 2 It responds to antihistaminic drugs 3 The same causes may provoke either urticaria or angioedema

Angioedemabusiness.industryfood and beveragesMast cellmedicine.diseasePathogenesischemistry.chemical_compoundmedicine.anatomical_structurechemistryimmune system diseasesImmunologyHereditary angioedemamedicineAntihistaminic drugscardiovascular diseasesmedicine.symptomskin and connective tissue diseasesbusinessHistamine
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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
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p Natural polyphenols as anti-inflammatory agents p

2009

Celiac Disease is a worldwide spread condition affecting 1:100-1:200 individuals. It is a permanent food intolerance to ingested gluten in genetically predisposed subjects. In this review we analyze the biochemical markers of the disease going from laboratory findings to histology passing through genetics. Gluten intolerance is a unique model of autoimmune disease in which we can recognize the main environmental factor (gluten) and the more complex genetic background. In additional way, serological markers for monitoring the disease and a safe and effective therapy (gluten free diet) are also available. In deed the environmental factor such as gluten intake is necessary to trigger the disea…

Anti-Inflammatory AgentsDiseaseHuman leukocyte antigenProtein Serine-Threonine KinasesModels BiologicalAntioxidantsGeneral Biochemistry Genetics and Molecular BiologyPathogenesisPhenolsmedicineHumansFlavonoidsInflammationchemistry.chemical_classificationAutoimmune diseaseMolecular StructureGeneral Immunology and Microbiologybusiness.industryPolyphenolsnutritional and metabolic diseasesGluten intolerancemedicine.diseaseGlutendigestive system diseasesFood intolerancechemistryCyclooxygenase 2ImmunologyCyclooxygenase 1Gluten freebusinessFrontiers in Bioscience
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Exploiting the Pleiotropic Antioxidant Effects of Established Drugs in Cardiovascular Disease.

2015

Cardiovascular disease is a leading cause of death and reduced quality of life worldwide. Arterial vessels are a primary target for endothelial dysfunction and atherosclerosis, which is accompanied or even driven by increased oxidative stress. Recent research in this field identified different sources of reactive oxygen and nitrogen species contributing to the pathogenesis of endothelial dysfunction. According to lessons from the past, improvement of endothelial function and prevention of cardiovascular disease by systemic, unspecific, oral antioxidant therapy are obviously too simplistic an approach. Source- and cell organelle-specific antioxidants as well as activators of intrinsic antiox…

Antioxidantmedicine.medical_treatmentGlucagon-Like PeptidesInflammationDiseaseReviewBiologymedicine.disease_causeCatalysisAntioxidantsendothelial dysfunctionInorganic ChemistryPathogenesislcsh:Chemistrycardiovascular diseasemedicineAnimalsHumansImmunologic FactorsPhysical and Theoretical ChemistryEndothelial dysfunctionMolecular Biologylcsh:QH301-705.5Spectroscopyglucagon-like peptide analogsCause of deathInflammationOrganic ChemistryGeneral Medicinemedicine.diseaseComputer Science ApplicationsClinical trialOxidative Stresslcsh:Biology (General)lcsh:QD1-999Cardiovascular DiseasesImmunologyEndothelium Vascularmedicine.symptomdipeptidyl peptidase-4 inhibitorsOxidative stressInternational journal of molecular sciences
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Overexpression of human hepatic lipase and ApoE in transgenic rabbits attenuates response to dietary cholesterol and alters lipoprotein subclass dist…

1999

Abstract —The effect of the expression of human hepatic lipase (HL) or human apoE on plasma lipoproteins in transgenic rabbits in response to dietary cholesterol was compared with the response of nontransgenic control rabbits. Supplementation of a chow diet with 0.3% cholesterol and 3.0% soybean oil for 10 weeks resulted in markedly increased levels of plasma cholesterol and VLDL and IDL in control rabbits as expected. Expression of either HL or apoE reduced plasma cholesterol response by 75% and 60%, respectively. The HL transgenic rabbits had substantial reductions in medium and small VLDL and IDL fractions but not in larger VLDL. LDL levels were also reduced, with a shift from larger, m…

Apolipoprotein EMalemedicine.medical_specialtyVery low-density lipoproteinTransgeneLipoproteinsCholesterol VLDLHypercholesterolemiaGene ExpressionPathogenesisAnimals Genetically ModifiedCholesterol Dietarychemistry.chemical_compoundApolipoproteins EInternal medicinemedicineAnimalsHumansTransgenesParticle SizeApolipoproteins BLagomorphabiologyCholesterolCholesterol HDLLipasebiology.organism_classificationEndocrinologyCholesterolchemistrylipoproteins apoE hepatic lipase rabbits transgeneLiverDiet Atherogeniclipids (amino acids peptides and proteins)Hepatic lipaseRabbitsCardiology and Cardiovascular MedicineLipoproteinArteriosclerosis, thrombosis, and vascular biology
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Immunopathogenesis of atherosclerosis: endotoxin accelerates atherosclerosis in rabbits on hypercholesterolemic diet.

2001

Background—On the basis of our concept that atherosclerosis has an immunopathological background, we tested whether activation of the innate immune system influences its progression.Methods and Results—Hypercholesterolemic (0.5% wt/wt diet) rabbits received either repeated intravenous injections of endotoxin (Escherichia colilipopolysaccharide 1.25 to 2.5 μg, once per week) or a self-limiting cutaneousStaphylococcus aureusinfection with or without a quinolone antibiotic. Measured laboratory parameters, including LDL and HDL cholesterols, were similar in the different groups of hypercholesterolemic animals. All endotoxin-treated animals developed transient episodes of fever after endotoxin a…

ArteriosclerosisInnate immunologyHypercholesterolemiaTriglycerides bloodPathogenesisCholesterol Dietarychemistry.chemical_compoundImmunityPhysiology (medical)MedicineAnimalsAortaTriglyceridesInnate immune systemCholesterolbusiness.industryDisease progressionCholesterol HDLCholesterol LDLImmunity InnateCholesterol bloodEndotoxinsDisease Models AnimalCholesterolchemistryImmunologyDisease ProgressionDiet AtherogenicFemaleStaphylococcal Skin InfectionsRabbitsCardiology and Cardiovascular MedicinebusinessCirculation
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Complement and atherogenesis: The unknown connection

1999

The question why low-density lipoprotein (LDL) stranded in the subendothelium of arteries should acquire the proinflammatory properties that initiate and sustain atherogenesis has puzzled researchers for decades. The most popular concept contends that oxidative processes are crucial because oxidized LDL (ox-LDL) produced in vitro has atherogenic properties and small amounts of it are found in atherosclerotic lesions. Recently, a possible role for vascular infections has also been considered because infectious agents, in particular Chlamydia pneumoniae, are sometimes present in the lesions. Here, evidence is summarized for a different concept of atherogenesis, which evolves from the fact tha…

ArteriosclerosisVascular diseaseInflammationGeneral MedicineChlamydia InfectionsChlamydophila pneumoniaeMacrophage ActivationBiologymedicine.diseaseProinflammatory cytokineLipoproteins LDLPathogenesischemistry.chemical_compoundImmune systemchemistryLow-density lipoproteinImmunologymedicineHumansMacrophagelipids (amino acids peptides and proteins)medicine.symptomComplement ActivationLipoproteinAnnals of Medicine
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A TNF-α Promoter Polymorphism Is Associated with Juvenile Onset Psoriasis and Psoriatic Arthritis

1997

Tumor necrosis factor-α is considered to be one of the important mediators in the pathogenesis of psoriasis. A strong association of juvenile onset psoriasis with the major histocompatibility complex encoded HLA-Cw6 antigen has been reported but it is unclear whether Cw6 itself or a closely linked gene is involved in the pathogenesis. This study has focused on the association of promoter polymorphisms of the major histocompatibility complex encoded tumor necrosis factor-α gene with psoriasis and psoriatic arthritis. Tumor necrosis factor-α promoter polymorphisms were sought by sequence-specific oligonucleotide hybridization and by direct sequencing in Caucasian patients with juvenile onset …

ArthritisCell BiologyDermatologyHuman leukocyte antigenBiologymedicine.diseaseMajor histocompatibility complexBiochemistrycytokinesmajor histocompatibility complexPathogenesisPsoriatic arthritisPsoriasisImmunologymedicinebiology.proteinTumor necrosis factor alphaHLA antigensAge of onsetMolecular Biologylinkage disequilibriumJournal of Investigative Dermatology
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