Search results for "POLYSACCHARIDE"

showing 10 items of 635 documents

Serum antibodies to Vibrio vulnificus biotype 3 lipopolysaccharide and susceptibility to disease caused by the homologous V. vulnificus biotype

2011

SUMMARYIn 1996 an outbreak of severe soft tissue infections caused byVibrio vulnificusunexpectedly erupted in fish consumers in Israel with relatively little morbidity in fish farmers. To test the hypothesis that recurrent exposure of fishermen to the virulent strain may have provided protection against severe or symptomatic disease, we investigated the association between the immune response toV. vulnificusbiotype 3 lipopolysaccharide (BT3 LPS) and disease susceptibility in fish farmers and fish consumers. Serum samples were tested for IgA and IgG of anti-BT3 LPS in fishermen and fish consumers who suffered fromV. vulnificusBT3 infections and their matched controls. Pre-existing levels of …

LipopolysaccharidesMaleSerumEpidemiologyVirulenceMicrobiologiaVibrio vulnificusImmunoglobulin GSerologyMicrobiologyVibrionaceaeVibrio Infectionsparasitic diseasesHumansIsraelVibrio vulnificusbiologyOutbreakMiddle Agedbiology.organism_classificationAntibodies BacterialImmunoglobulin AInfectious DiseasesCase-Control StudiesImmunoglobulin GVibrio InfectionsImmunologybiology.proteinFemaleDisease SusceptibilityAntibody
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Intravitreal injection of bevacizumab induces inflammatory alterations in a uveitis experimental model.

2010

PurposeBevacizumab is currently used as an intravitreal agent in the treatment of inflammatory-associated eye diseases. The aim of the current study is to explore the effects of the intravitreal injection of bevacizumab on aqueous humour cytokines and chemokines in an experimental uveitis model.MethodsEndotoxin-induced uveitis was induced in rats by footpad injections. Bevacizumab was administered by intravitreal injection (75 μg in 3–μL samples) and different chemokine and cytokine proteins were quantified in aqueous humor.ResultsIntravitreal administration of bevacizumab led to a several-fold increase of RANTES, MCP-1, and IFN-γ concentrations in aqueous humor of endotoxin-treated rats.Co…

LipopolysaccharidesMaleVascular Endothelial Growth Factor AChemokinegenetic structuresBevacizumabmedicine.medical_treatmentInflammationAngiogenesis InhibitorsEnzyme-Linked Immunosorbent AssayPharmacologyAntibodies Monoclonal HumanizedAqueous HumorUveitisInterferon-gammaMedicineAnimalsChemokine CCL5Chemokine CCL2biologybusiness.industryAqueous humourGeneral MedicineIntravitreal administrationmedicine.diseaseeye diseasesRatsBevacizumabOphthalmologyDisease Models AnimalCytokineRats Inbred LewMonoclonalIntravitreal Injectionsbiology.proteinCytokinessense organsmedicine.symptombusinessUveitismedicine.drugEuropean journal of ophthalmology
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Beta- and gamma-melanocortins inhibit lipopolysaccharide induced nitric oxide production in mice brain.

2003

The pro-opiomelanocortin-derived peptide alpha-melanocyte stimulating hormone (alpha-MSH) mediates many diverse physiological actions, including anti-inflammatory and immunomodulatory effects. However, little is known about the physiological roles of the other melanocortins, beta- and gamma-MSH. Here, we investigated the effects of melanocortin peptides in an in vivo neuroinflammation model. Six hours following intracisternal (i.c.) administration of 10 microg lipopolysaccharide (LPS) to mice a five-fold increase in the nitric oxide (NO) level was seen in the animals' brains, when detected by electron paramagnetic resonance (EPR). All tested melanocortins, alpha-, beta-, gamma1- and gamma2-…

LipopolysaccharidesMaleendocrine systemmedicine.medical_specialtyLipopolysaccharideCentral nervous systemInflammationPharmacologyBiologyNitric OxideNitric oxidechemistry.chemical_compoundMicegamma-MSHIn vivoInternal medicinebeta-MSHmedicineAnimalsMolecular BiologyNeuroinflammationMelanocortinsFeedback PhysiologicalMice Inbred ICRintegumentary systemDose-Response Relationship DrugGeneral NeuroscienceElectron Spin Resonance SpectroscopyBrainDisease Models Animalmedicine.anatomical_structureEndocrinologychemistryalpha-MSHNeurology (clinical)Melanocortinmedicine.symptomInflammation Mediatorshormones hormone substitutes and hormone antagonistsDevelopmental BiologySignal TransductionBrain research
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Beta-MSH inhibits brain inflammation via MC(3)/(4) receptors and impaired NF-kappaB signaling.

2005

The anti-inflammatory effects of melanocortin peptides have been demonstrated in different inflammation models. This is the first report describing the molecular mechanisms for the beta-MSH-induced suppression of bacterial lipopolisaccharide (LPS)-caused brain inflammation. We found that beta-MSH suppresses LPS-induced nuclear translocation of the transcription factor NF-kappaB, and inhibits the expression of inducible nitric oxide synthase, and the following nitric oxide overproduction in the brain, in vivo. Moreover, administering the preferentially MC(4) receptor selective antagonist HS014 blocked completely these effects, suggesting a tentative MC(4) receptor mediated mechanism of actio…

LipopolysaccharidesMalemedicine.medical_specialtyImmunologyNitric Oxide Synthase Type IIInflammationElectrophoretic Mobility Shift AssayNitric OxidePeptides CyclicNitric oxidechemistry.chemical_compoundMiceInternal medicinebeta-MSHmedicineImmunology and AllergyAnimalsDrug InteractionsReceptorBrain ChemistryMice Inbred ICRbiologyDose-Response Relationship DrugImmunochemistryElectron Spin Resonance SpectroscopyNF-kappa BNF-κBHormonesCell biologyNitric oxide synthaseDisease Models AnimalEndocrinologyNeurologyMechanism of actionchemistrybiology.proteinEncephalitisReceptor Melanocortin Type 4Neurology (clinical)medicine.symptomMelanocortinSignal transductionhormones hormone substitutes and hormone antagonistsReceptor Melanocortin Type 3Signal TransductionJournal of neuroimmunology
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Hepatic over-expression of TGF-beta1 promotes LPS-induced inflammatory cytokine secretion by liver cells and endotoxemic shock.

2005

Transforming growth factor-beta (TGF-beta) is an important suppressor of inflammation. However, TGF-beta has also been found to promote secretion of inflammatory cytokines, and transgenic mice, which constitutively express TGF-beta in liver, have been found to be more susceptible to endotoxemia. To approach this apparent paradox, we investigated the role of hepatic TGF-beta1 in endotoxemia by utilising inducible TGF-beta1-transgenic mice that express TGF-beta1 under control of the C-reactive protein promoter. In contrast to non-transgenic littermates, administration of lipopolysaccharide (LPS) induced strongly increased expression of TGF-beta and acute phase proteins in the TGF-beta1-transg…

LipopolysaccharidesMalemedicine.medical_specialtyLipopolysaccharidemedicine.medical_treatmentImmunologyInflammationMice TransgenicBiologyProinflammatory cytokineTransforming Growth Factor beta1chemistry.chemical_compoundMiceImmune systemTransforming Growth Factor betaInternal medicinemedicineImmunology and AllergyAnimalsSecretionAcute-Phase ReactionCells CulturedInterleukin-6Acute-phase proteinEndotoxemiaCytokineEndocrinologychemistryHepatocytesCytokine secretionmedicine.symptomInflammation MediatorsImmunology letters
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Whole blood endotoxin responsiveness in patients with chronic heart failure: the importance of serum lipoproteins.

2005

Background Endotoxin [lipopolysaccharide (LPS)] may be an important stimulus for cytokine release in patients with chronic heart failure (CHF). We sought to investigate the relationship between whole blood endotoxin responsiveness and serum lipoprotein concentrations. It is not known if low-dose LPS is sufficient to stimulate immune activation. Methods and results Whole blood from 32 CHF patients (mean age 66±2 years, NYHA class 2.7±0.2, five female) and 11 healthy control subjects (mean age 47±4 years, six female) was stimulated with LPS at nine different concentrations (0.001 to 10 ng/mL), and tumor necrosis factor (TNF-α) release was quantified. Reference standard endotoxin at concentrat…

LipopolysaccharidesMalemedicine.medical_specialtyLipopolysaccharidemedicine.medical_treatmentLipoproteinsEnzyme-Linked Immunosorbent Assaychemistry.chemical_compoundIn vivoInternal medicinemedicineHumansWhole bloodAgedHeart Failurebusiness.industryTumor Necrosis Factor-alphaMiddle Agedmedicine.diseaseEndocrinologyCytokinechemistryHeart failureTumor necrosis factor alphaFemaleCardiology and Cardiovascular MedicinebusinessEx vivoLipoproteinEuropean journal of heart failure
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Transcriptional up-regulation of nNOS in the dorsal vagal complex during low endotoxemia

2005

The present study analyses the expression and distribution of neuronal nitric oxide synthase (nNOS) in the brainstem of animals pre-treated with Escherichia coli or Helicobacter pylori LPS, at doses that modulate gastric motor function. Systemic administration of H. pylori LPS prevented in a dose-dependent manner (5, 40 and 100 microg kg(-1), i.v.) the increase in intragastric pressure induced by 2-deoxy-D-glucose (200 mg kg(-1), i.v.) in urethane-anaesthetized rats. Quantitative analysis showed a significant increase in the amount of nNOS mRNA induced by E. coli or H. pylori LPS (2 h later), in a segment of the brainstem containing the dorsal vagal complex (DVC). Immunohistochemical studie…

LipopolysaccharidesMalemedicine.medical_specialtyNerve Tissue ProteinsNitric Oxide Synthase Type Imedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyRats Sprague-DawleyDownregulation and upregulationInternal medicineEscherichia coliPressuremedicineAnimalsGeneral Pharmacology Toxicology and PharmaceuticsEscherichia coliMessenger RNAbiologyStomachVagus NerveGeneral MedicineHelicobacter pyloribiology.organism_classificationEndotoxemiaRatsUp-RegulationEndocrinologyDorsal motor nucleusAnesthesiaSystemic administrationImmunohistochemistryBrainstemNitric Oxide SynthaseBrain StemLife Sciences
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Glucose-independent improvement of vascular dysfunction in experimental sepsis by dipeptidyl-peptidase 4 inhibition.

2012

Aims Dipeptidyl peptidase-4 (DPP-4) inhibitors are a novel class of drugs for the treatment of hyperglycaemia. Preliminary evidence suggests that their antioxidant and anti-inflammatory effects may have beneficial effects on the cardiovascular complications of diabetes. In the present study, we investigate in an experimental sepsis model whether linagliptin exerts pleiotropic vascular effects independent of its glucose-lowering properties. Methods and results Linagliptin (83 mg/kg chow for 7days) was administered in a rat model of lipopolysaccharide (LPS) (10 mg/kg, single i.p. dose/24 h)-induced sepsis. Vascular relaxation, reactive oxygen species (ROS) formation, expression of NADPH oxida…

LipopolysaccharidesMalemedicine.medical_specialtyPhysiologyNeutrophilsAdministration OralVasodilationLinagliptinBiologyLinagliptinAntioxidantsProinflammatory cytokineSepsisPhysiology (medical)Internal medicineSepsismedicineLeukocytesAnimalsHumansEndothelial dysfunctionRats WistarDipeptidyl peptidase-4Respiratory BurstDipeptidyl-Peptidase IV InhibitorsNADPH oxidasemedicine.diseaseRespiratory burstRatsVasodilationOxidative StressEndocrinologyPurinesbiology.proteinQuinazolinesCardiology and Cardiovascular MedicineDiabetic Angiopathiesmedicine.drugCardiovascular research
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Involvement of neuronal processes and nitric oxide in the inhibition by endotoxin of pentagastrin-stimulated sastric acid secretion

1994

Administration of E. coli endotoxin (1 mg kg-1, i.v.) abolished the acid response induced by the i.v. infusion of pentagastrin (8 micrograms kg-1 h-1) in the continuously perfused stomach of the anaesthetized rat. Local serosal application of tetrodotoxin (36 ng per rat) completely restored acid responses to pentagastrin in endotoxin-treated rats. However, pretreatment with atropine (0.5 mg kg-1, s.c.), capsaicin (20, 30, and 50 mg kg-1, s.c. 2 weeks before the study) or guanethidine (16 mg kg-1, s.c. 3 and 16h before) did not influence the inhibitory effects of endotoxin. Continuous i.v. infusion with NG-nitro arginine methyl ester (L-NAME, 10 mg kg-1 h-1) restored the secretory responses …

LipopolysaccharidesMalemedicine.medical_specialtyTetrodotoxinPeptide hormoneBiologyArginineNitric OxideNitric oxideGastric AcidPhenylephrinechemistry.chemical_compoundInternal medicineEscherichia colimedicineAnimalsDrug InteractionsRats WistarInfusions IntravenousGuanethidineNeuronsPharmacologyStomachGeneral MedicineRatsEndotoxinsPentagastrinNG-Nitroarginine Methyl EsterEndocrinologyMechanism of actionchemistryGastrointestinal hormoneGastric MucosaCapsaicinTetrodotoxinFemalePentagastrinmedicine.symptommedicine.drugNaunyn-Schmiedeberg's Archives of Pharmacology
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ttCH, a selective inhibitor of inducible nitric oxide synthase expression with antiarthritic properties

2003

In a previous work, we investigated the effects of a series of dimethoxy- and trimethoxychalcone derivatives, with various patterns of fluorination, on nitric oxide production in lipopolysaccharide-stimulated murine RAW 264.7 cells. The present study was designed to determine if 2,4,6-trimethoxy-2'-trifluoromethylchalcone (ttCH) could modulate the production of nitric oxide (NO) and/or prostaglandins in vitro and in vivo. On the mouse macrophage cell line RAW 264.7, ttCH inhibited dose-dependently NO and prostaglandin E(2) production, with IC(50) in the micromolar range. This compound had no direct inhibitory effect on inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 activities. …

LipopolysaccharidesMalemedicine.medical_treatmentBlotting WesternNitric Oxide Synthase Type IIPharmacologyCarrageenanNitric OxideDinoprostoneCell LineNitric oxideMicechemistry.chemical_compoundIn vivomedicineAnimalsEdemaEnzyme InhibitorsProstaglandin E2InflammationPharmacologybiologyChemistryMacrophagesAnti-Inflammatory Agents Non-SteroidalBiological activityArthritis ExperimentalHindlimbRatsCarrageenanIsoenzymesRadiographyNitric oxide synthaseMechanism of actionBiochemistryCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesRats Inbred Lewbiology.proteinFemaleNitric Oxide Synthasemedicine.symptomProstaglandin Emedicine.drugEuropean Journal of Pharmacology
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