Search results for " inflammation."

showing 10 items of 623 documents

Ciona intestinalis interleukin 17-like genes expression is upregulated by LPS challenge

2015

In humans, IL-17 is a proinflammatory cytokine that plays a key role in the clearance of extracellular bacteria promoting cell infiltration and production of several cytokines and chemokines. Here, we report on three Ciona intestinalis IL-17 homologues (CiIL17-1, CiIL17-2, CiIL17-3). The gene organisation, phylogenetic tree and modelling supported the close relationship with the mammalian IL-17A and IL-17F suggesting that the C. intestinalis IL-17 genes share a common ancestor in the chordate lineages. Real time PCR analysis showed a prompt expression induced by LPS inoculation suggesting that they are involved in the first phase of inflammatory response. In situ hybridization assays disclo…

LipopolysaccharidesChemokineLPSHemocytesAscidianMolecular Sequence DataImmunologySettore BIO/05 - ZoologiaIn situ hybridizationBiologyGranulocyteProinflammatory cytokineExtracellularmedicineAnimalsHumansProtein IsoformsCiona intestinalisAmino Acid SequenceGenePhylogenyInflammationBase SequenceInterleukin-17InterleukinSequence Analysis DNAbiology.organism_classificationCiona intestinalisCell biologyinterleukin IL17 hemocytemedicine.anatomical_structureImmunologybiology.proteinAscidian; interleukin IL17 hemocyte; inflammation; LPS; Ciona intestinalisSequence AlignmentDevelopmental Biology
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Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide …

2014

Macrophages come across active prostaglandin (PG) metabolism during inflammation, shunting early production of pro-inflammatory towards anti-inflammatory mediators terminating the process. This work for the first time provides evidence that a phytochemical may modulate the arachidonate (AA) metabolism in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages, promoting the ultimate formation of anti-inflammatory cyclopentenone 15deoxy-PGJ2. Added 1 h before LPS, indicaxanthin from Opuntia Ficus Indica prevented activation of nuclear factor-κB (NF-κB) and over-expression of PGE2 synthase-1 (mPGES-1), but up-regulated cyclo-oxygenase-2 (COX-2) and PGD2 synthase (H-PGDS), with final product…

LipopolysaccharidesLipid PeroxidesLipopolysaccharidePyridinesPhytochemicalsClinical BiochemistryProstaglandinIndicaxanthinmedicine.disease_causeBiochemistryCell LineMiceStructure-Activity Relationshipchemistry.chemical_compoundmedicineAnimalslcsh:QH301-705.5Inflammationlcsh:R5-920Arachidonic AcidNADPH oxidaseDose-Response Relationship DrugLipid peroxidebiologyMacrophagesOrganic ChemistryOpuntiaMetabolismOxidantsPro-oxidantBetaxanthinslcsh:Biology (General)chemistryBiochemistryOxidative stressFruitIndicaxanthin Phytochemicals Eicosanoids Inflammation Oxidative stress.Prostaglandinsbiology.proteinEicosanoidslipids (amino acids peptides and proteins)lcsh:Medicine (General)IndicaxanthinOxidative stressResearch PaperRedox Biology
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Immune Cell Toll-like Receptor 4 Mediates the Development of Obesity- and Endotoxemia-Associated Adipose Tissue Fibrosis

2014

International audience; Adipose tissue fibrosis development blocks adipocyte hypertrophy and favors ectopic lipid accumulation. Here, we show that adipose tissue fibrosis is associated with obesity and insulin resistance in humans and mice. Kinetic studies in C3H mice fed a high-fat diet show activation of macrophages and progression of fibrosis along with adipocyte metabolic dysfunction and death. Adipose tissue fibrosis is attenuated by macrophage depletion. Impairment of Toll-like receptor 4 signaling protects mice from obesity-induced fibrosis. The presence of a functional Toll-like receptor 4 on adipose tissue hematopoietic cells is necessary for the initiation of adipose tissue fibros…

LipopolysaccharidesMESH: Signal TransductionMESH: InflammationMESH : Toll-Like Receptor 4Adipose tissueMESH : AdipocytesMESH : LipopolysaccharidesMicechemistry.chemical_compoundFibrosisAdipocyteAdipocytes[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMESH: ObesityMESH: Animalslcsh:QH301-705.5Mice Inbred C3HToll-like receptorMESH : Diet High-FatMESH: Toll-Like Receptor 43. Good healthMESH: Insulin ResistanceAdipose TissueMESH: FibrosisMESH : Fibrosis[SDV.IMM]Life Sciences [q-bio]/ImmunologyMESH : ObesityMESH : Insulin ResistanceMESH: Adipose TissueSignal Transductionmedicine.medical_specialty[SDV.IMM] Life Sciences [q-bio]/ImmunologyAdipose tissue macrophagesBiologyDiet High-FatMESH : Adipose TissueGeneral Biochemistry Genetics and Molecular BiologyImmune systemMESH : Mice Inbred C3HInternal medicineMESH : MicemedicineAnimalsHumansObesityMESH: Mice Inbred C3HMESH: MiceMESH: AdipocytesInflammationMESH : Signal TransductionMESH : InflammationMESH: HumansMESH : EndotoxemiaMESH : Humans3T3-L1medicine.diseaseFibrosisMESH : Disease Models AnimalEndotoxemiaToll-Like Receptor 4Disease Models AnimalMESH: Diet High-FatEndocrinologylcsh:Biology (General)chemistryMESH: EndotoxemiaMESH : AnimalsInsulin ResistanceMESH: Disease Models AnimalMESH: LipopolysaccharidesAdipocyte hypertrophyCell Reports
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Time Response of Oxidative/Nitrosative Stress and Inflammation in LPS-Induced Endotoxaemia—A Comparative Study of Mice and Rats

2017

Sepsis is a severe and multifactorial disease with a high mortality rate. It represents a strong inflammatory response to an infection and is associated with vascular inflammation and oxidative/nitrosative stress. Here, we studied the underlying time responses in the widely used lipopolysaccharide (LPS)-induced endotoxaemia model in mice and rats. LPS (10 mg/kg; from Salmonella Typhosa) was intraperitoneally injected into mice and rats. Animals of every species were divided into five groups and sacrificed at specific points in time (0, 3, 6, 9, 12 h). White blood cells (WBC) decreased significantly in both species after 3 h and partially recovered with time, whereas platelet decrease did no…

LipopolysaccharidesMale0301 basic medicinesepsis; time response; inflammation; oxidative stress; endotoxaemia; mouse; ratLipopolysaccharideNitric Oxide Synthase Type IIBacteremia030204 cardiovascular system & hematologymedicine.disease_causelcsh:ChemistrysepsisendotoxaemiaHemoglobinsLeukocyte CountMicechemistry.chemical_compound0302 clinical medicineoxidative stressratPlateletlcsh:QH301-705.5SpectroscopyGeneral MedicineComputer Science ApplicationsRespiratory burstP-SelectinSalmonella Infectionsmedicine.symptommedicine.medical_specialtyVascular Cell Adhesion Molecule-1InflammationOxidative phosphorylationArticleCatalysisInorganic ChemistrySepsis03 medical and health sciencesSpecies Specificitytime responseInternal medicineReaction TimemedicineAnimalsRats WistarPhysical and Theoretical ChemistryMolecular BiologymouseInterleukin-6Platelet CountTumor Necrosis Factor-alphabusiness.industryOrganic Chemistrymedicine.diseaseRatsMice Inbred C57BL030104 developmental biologyEndocrinologylcsh:Biology (General)lcsh:QD1-999chemistryinflammationImmunologyHemoglobinbusinessOxidative stressInternational Journal of Molecular Sciences
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Inflamed adult pharynx tissues and swimming larva of Ciona intestinalis share CiTNFalpha-producing cells.

2010

In situ hybridisation and immunohistochemistry analyses have shown that the Ciona intestinalis tumour necrosis factor alpha gene (CiTNFalpha), which has been previously cloned and sequenced, is expressed either during the inflammatory pharynx response to lipopolysaccharide (LPS) or during the swimming larval phase of development. Granulocytes with large granules and compartment/morula cells are CiTNFalpha-producing cells in both inflamed pharynx and larvae. Pharynx vessel endothelium also takes part in the inflammatory response. Haemocyte nodules in the vessel lumen or associated with the endothelium suggest the involvement of CiTNFalpha in recruiting lymphocyte-like cells and promoting the…

LipopolysaccharidesPathologymedicine.medical_specialtyHistologyHemocytesEndotheliumEvolutionMesenchymeSettore BIO/05 - ZoologiaInflammationIn situ hybridizationBiologyAscidia Ciona intestinalisPathology and Forensic MedicinemedicineAnimalsCiona intestinalisTumour necrosis factor; Pharynx; Inflammation; Haemocytes; Larval development; Innate immunity; Evolution; Ascidia Ciona intestinalisIn Situ Hybridization FluorescencePhylogenyInflammationInnate immunityInnate immune systemTumor Necrosis Factor-alphaPharynxMetamorphosis BiologicalHaemocytePharyngitisCell Biologybiology.organism_classificationImmunohistochemistryCiona intestinalismedicine.anatomical_structureLarval developmentLarvaImmunohistochemistryPharynxmedicine.symptomTumour necrosis factorGranulocytesCell and tissue research
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LPS challenge regulates gene expression and tissue localization of a Ciona intestinalis gene through an alternative polyadenylation mechanism.

2013

A subtractive hybridization strategy for the identification of differentially expressed genes was performed between LPS-challenged and naive Ciona intestinalis. This strategy allowed the characterization of two transcripts (Ci8short and Ci8long) generated by the use of two Alternative Polyadenylation sites. The Ci8long transcript contains a protein domain with relevant homology to several components of the Receptor Transporting Protein (RTP) family not present in the Ci8short mRNA. By means of Real Time PCR and Northern Blot, the Ci8short and Ci8long transcripts showed a different pattern of gene expression with the Ci8short mRNA being strongly activated after LPS injection in the pharynx. …

LipopolysaccharidesPolyadenylationCiona intestinaliSettore BIO/05 - Zoologialcsh:MedicineGene ExpressionBiochemistryGene expressionGene Orderlcsh:Science3' Untranslated RegionsPhylogenyIn Situ HybridizationRegulation of gene expressionMultidisciplinaryInnate ImmunityCiona intestinalisPhylogeneticsProtein TransportCytochemistryResearch ArticleDNA ComplementaryMolecular Sequence DataImmunologyIn situ hybridizationBiologyPolyadenylationModel OrganismsGeneticsAnimalsCiona intestinalisEvolutionary SystematicsNorthern blotAmino Acid SequenceRNA MessengerBiologyEvolutionary BiologyBase SequenceThree prime untranslated regionlcsh:RImmunityComputational BiologyProteinsImmune Defensebiology.organism_classificationMolecular biologyGenesinflammationSuppression subtractive hybridizationlcsh:Q5' Untranslated RegionsCiona intestinalis; inflammationSequence AlignmentPloS one
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The prophenoloxidase system is activated during the tunic inflammatory reaction of Ciona intestinalis

2008

Phenoloxidase (PO) activity was examined in the tunic tissue of Ciona intestinalis following lipopolysaccharide (LPS) intratunic injection. Tunic homogenate supernatant (THS), assayed with the Dopa-MBTH reaction, displayed Ca(2+)-independent PO activity that was raised by LPS and further enhanced by proteases. Specific inhibitors (tropolone, phenylthiourea, diethylthiocarbamate) supported the specificity of the reaction. Assay with soybean trypsin inhibitor showed that, in the tunic, PO activation with trypsin was not significantly inhibited suggesting that proteases diverse from serine proteases were involved. In vivo experiments were carried out by injecting isosmotic medium or LPS, and T…

LipopolysaccharidesProteasesHistologyBlotting WesternSettore BIO/05 - ZoologiaEnzyme-Linked Immunosorbent AssayPathology and Forensic MedicinemedicineAnimalsCiona intestinalisInflammationchemistry.chemical_classificationEnzyme PrecursorsbiologyKunitz STI protease inhibitorprophenoloxidase Ciona intestinalisCell BiologyProphenoloxidasebiology.organism_classificationTrypsinImmunohistochemistryMolecular biologyIn vitroCiona intestinalisUp-RegulationCionaEnzymechemistryPhenoloxidase . Hemocyte . Tunic . Inflammation . Lipopolysaccharide . SDS-polyacrylamide gel electrophoresis . Ciona intestinalisElectrophoresis Polyacrylamide GelCatechol Oxidasemedicine.drugCell and Tissue Research
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Ciona intestinalis galectin (CiLgals-a and CiLgals-b) genes are differentially expressed in endostyle zones and challenged by LPS

2015

Abstract Immunohistochemical and in situ hybridization assays were performed to answer the question whether the endostyle, that is the initial gastro-intestinal trait of Ciona intestinalis pharynx, is involved in galectin (CiLgals-a and CiLgals-b) production during the pharynx inflammatory response to LPS inoculation. Specific anti-CiLgal-a and anti-CiLgals-b antibodies, and oligonucleotide probes, that mark inflammatory hemocytes inside the pharynx vessels and vessel epithelium as shown by a previous paper, were assayed on endostyle histological sections. For the first time, we show that galectins are produced by endostyle zones, and both CiLgals-a and –b genes are upregulated by LPS. CiLg…

LipopolysaccharidesSignal peptideLPSAscidianGalectinsOligonucleotidesSettore BIO/05 - ZoologiaIn situ hybridizationAquatic ScienceBiologyendostyleDownregulation and upregulationotorhinolaryngologic diseasesmedicineExtracellularAnimalsEnvironmental ChemistryCiona intestinalisIn Situ HybridizationGalectinAscidian Galectin Endostyle Inflammation Ciona intestinalisgalectinGeneral Medicinebiology.organism_classificationImmunohistochemistryMolecular biologyEpitheliumCiona intestinalismedicine.anatomical_structureItalyinflammationImmunologyPharynxEndostyle
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Quaking and miR-155 interactions in inflammation and leukemogenesis.

2015

Quaking (QKI) is a tumor-suppressor gene encoding a conserved RNA-binding protein, whose expression is downregulated in several solid tumors. Here we report that QKI plays an important role in the immune response and suppression of leukemogenesis. We show that the expression of Qki is reduced in lipopolysaccharide (LPS)-challenged macrophages, suggesting that Qki is a key regulator of LPS signaling pathway. Furthermore, LPS-induced downregulation of Qki expression is miR-155-dependent. Qki overexpression impairs LPS-induced phosphorylation of JNK and particularly p38 MAPKs, in addition to increasing the production of anti-inflammatory cytokine IL-10. In contrast, Qki ablation decreases Fas …

LipopolysaccharidesTime Factorsmedicine.medical_treatmentmedicine.disease_causeTransgenicMiceInnatePhosphorylationChronicB-LymphocytesLeukemiaRNA-Binding ProteinsU937 CellsLymphocyticCell biologyCytokineOncologyPhosphorylationCytokinesCLL; Glioblastoma; Inflammation; MiR-155; QKI; Animals; Apoptosis Regulatory Proteins; B-Lymphocytes; Case-Control Studies; Cytokines; Humans; Immunity Innate; Inflammation; Leukemia Lymphocytic Chronic B-Cell; Lipopolysaccharides; Macrophages; Mice; Mice Transgenic; MicroRNAs; Mitogen-Activated Protein Kinases; Phosphorylation; RAW 264.7 Cells; RNA-Binding Proteins; Signal Transduction; Time Factors; Transfection; U937 Cells; OncologySignal transductionMitogen-Activated Protein KinasesSignal Transductionp38 mitogen-activated protein kinasesOncology and CarcinogenesisMice TransgenicTransfectionNOmiR-155miR-155Downregulation and upregulationmicroRNAmedicineAnimalsHumansInflammationQKIbusiness.industryMacrophagesB-CellImmunityglioblastomaLeukemia Lymphocytic Chronic B-CellImmunity InnateMicroRNAsRAW 264.7 CellsCase-Control StudiesImmunologyCarcinogenesisbusinessApoptosis Regulatory ProteinsCLLPriority Research Paper
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New clinical and pathophysiological perspectives defining the trajectory of cirrhosis

2021

Traditionally, the complications of cirrhosis, namely variceal bleeding, ascites and hepatic encephalopathy, were thought to result predominantly from circulatory dysfunction and altered organ perfusion arising as a result of portal hypertension. Over the past 20 years, large, international prospective studies have indicated the importance of systemic inflammation and organ immunopathology as additional determinants of organ dysfunction in cirrhosis, which not only manifests in the liver, brain, circulation and the kidneys, but also the immune system, gut, muscles, adrenal glands, reproductive organs, heart and lungs. This review provides an overview of the traditional and emerging concepts…

Liver Cirrhosis0301 basic medicinemedicine.medical_specialtyVaricesCirrhosisSystemic inflammationImmune System Phenomena03 medical and health sciences0302 clinical medicineImmunopathologyAscitesmedicineAcute on chronic liver failureHumansDecompensationIntensive care medicineHepatic encephalopathyHepatic encephalopathyInflammationHepatologybusiness.industryResearchOrgan dysfunctionGastroenterologyAscitesAcute on chronic liver failure; Ascites; Cirrhosis; Hepatic encephalopathy; Infection; Inflammation; Varicesmedicine.disease030104 developmental biologyCirrhosisDisease ProgressionPortal hypertension030211 gastroenterology & hepatologymedicine.symptombusinessInfection
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