Search results for "Trinitrobenzenes"

showing 10 items of 33 documents

The activation of Wnt signaling by a STAT6-dependent macrophage phenotype promotes mucosal repair in murine IBD

2016

The complete repair of the mucosa constitutes a key goal in inflammatory bowel disease (IBD) treatment. The Wnt signaling pathway mediates mucosal repair and M2 macrophages that coordinate efficient healing have been related to Wnt ligand expression. Signal transducer and activator of transcription 6 (STAT6) mediates M2 polarization in vitro and we hypothesize that a STAT6-dependent macrophage phenotype mediates mucosal repair in acute murine colitis by activating the Wnt signaling pathway. Our results reveal an impaired mucosal expression of M2 macrophage-associated genes and delayed wound healing in STAT6(-/-) mice treated with 2,4,6-trinitrobenzenesulfonic acid (TNBS). These mice also ex…

0301 basic medicineCellular differentiationImmunologyBiology03 medical and health sciencesMice0302 clinical medicineImmunology and AllergyAnimalsHumansIntestinal MucosaCells CulturedSTAT6Mice KnockoutMice Inbred BALB CWound HealingWnt signaling pathwayLGR5LRP5Cell DifferentiationColitisInflammatory Bowel DiseasesCell biologyWnt Proteins030104 developmental biologyPhenotypeTrinitrobenzenesulfonic AcidImmunologySTAT proteinMacrophages PeritonealSignal transductionWound healingSTAT6 Transcription Factor030215 immunologySignal Transduction
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CD16+ Macrophages Mediate Fibrosis in Inflammatory Bowel Disease.

2017

Background and Aims Fibrosis is a common complication of Crohn's disease [CD], and is related to dysregulated tissular repair following inflammation, in which macrophages play a central role. We have previously observed that STAT6-/- mice present delayed mucosal recovery after 2,4,6-trinitrobenzenesulfonic acid [TNBS]-induced colitis due to a deficiency in reparatory interleukin-4 [IL4]/STAT6-dependent M2 macrophages, which can be reverted by the exogenous transfer of this cell type. In the present study, we analyse the role of STAT6-dependent macrophages in intestinal fibrosis. Methods Colitis was induced by weekly intra-rectal administration of TNBS [6 weeks] to STAT6-/- mice and wild-typ…

0301 basic medicineMaleCell CountInflammatory bowel diseaseMiceCrohn DiseaseFibrosisMacrophageIntestinal MucosaCells CulturedMice Knockouteducation.field_of_studyMice Inbred BALB Cintegumentary systemGastroenterologyGeneral MedicineColitisColonic NeoplasmsFemalemedicine.symptomMannose ReceptorAdultAdolescentColonPopulationInflammationReceptors Cell SurfaceCD1603 medical and health sciencesYoung AdultProto-Oncogene Proteinsparasitic diseasesmedicineAnimalsHumansLectins C-TypeColitiseducationInterleukin 4business.industryMacrophagesReceptors IgGmedicine.diseaseFibrosisWnt Proteins030104 developmental biologyMannose-Binding LectinsTrinitrobenzenesulfonic AcidImmunologyInterleukin-4businessSTAT6 Transcription FactorJournal of Crohn'scolitis
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Protective Effect of Pogostone on 2,4,6-Trinitrobenzenesulfonic Acid-Induced Experimental Colitis via Inhibition of T Helper Cell

2017

Inflammatory bowel disease (IBD) is a chronic immune-related disease mainly caused by the disequilibrium of T helper (Th) cell paradigm? Pogostone (PO) is one of the major chemical constituents of Pogostemon cablin (Blanco) Benth. The present study aims to investigate the potential benefit of PO against IBD in a 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced experimental colitis model. PO treatment by enema significantly brought down the disease activity index (DAI) of the TNBS-challenged rats, which was manifested by the ameliorated inflammatory features including ulceration, adhesion, and edema. Hematoxylin-eosin (HE) staining and immunohistochemistry analysis showed that PO effectivel…

0301 basic medicineexperimental colitisCellPharmacologyInflammatory bowel diseaseProinflammatory cytokine03 medical and health scienceschemistry.chemical_compound246-Trinitrobenzenesulfonic acidEdemamedicinePharmacology (medical)T helper cellOriginal ResearchPharmacologybiologyCell growthbusiness.industrylcsh:RM1-950pogostoneT helper cellmedicine.diseaseTNBSanti-inflammationdigestive system diseaseslcsh:Therapeutics. Pharmacology030104 developmental biologymedicine.anatomical_structurechemistryMyeloperoxidaseImmunologybiology.proteinmedicine.symptombusinessFrontiers in Pharmacology
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The transcription factor IFN regulatory factor–4 controls experimental colitis in mice via T cell–derived IL-6

2008

The proinflammatory cytokine IL-6 seems to have an important role in the intestinal inflammation that characterizes inflammatory bowel diseases (IBDs) such as Crohn disease and ulcerative colitis. However, little is known about the molecular mechanisms regulating IL-6 production in IBD. Here, we assessed the role of the transcriptional regulator IFN regulatory factor-4 (IRF4) in this process. Patients with either Crohn disease or ulcerative colitis exhibited increased IRF4 expression in lamina propria CD3+ T cells as compared with control patients. Consistent with IRF4 having a regulatory function in T cells, in a mouse model of IBD whereby colitis is induced in RAG-deficient mice by transp…

AdultCD4-Positive T-LymphocytesMaleAdoptive cell transferRecombinant Fusion ProteinsT-LymphocytesCD3T cellAdoptive Transfer; Adult; Animals; Apoptosis; CD4-Positive T-Lymphocytes; Colitis; Cytokines; DNA-Binding Proteins; Female; Gene Expression Regulation; Humans; Inflammatory Bowel Diseases; Interferon Regulatory Factors; Interleukin-6; Intestinal Mucosa; Male; Mice; Mice Inbred C57BL; Mice Knockout; Middle Aged; Oxazolone; Receptors Interleukin-6; Recombinant Fusion Proteins; T-Lymphocytes; Trinitrobenzenesulfonic AcidApoptosisProinflammatory cytokineMiceIntestinal mucosamedicineAnimalsHumansIntestinal MucosaColitisInterleukin 6Mice KnockoutbiologyInterleukin-6OxazoloneGeneral MedicineMiddle AgedColitisInflammatory Bowel Diseasesmedicine.diseaseAdoptive TransferReceptors Interleukin-6Ulcerative colitisDNA-Binding ProteinsMice Inbred C57BLmedicine.anatomical_structureGene Expression RegulationTrinitrobenzenesulfonic AcidInterferon Regulatory FactorsImmunologybiology.proteinCytokinesFemaleResearch ArticleJournal of Clinical Investigation
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Local administration of antisense phosphorothioate oligonucleotides to the p65 subunit of NF-kappa B abrogates established experimental colitis in mi…

1996

Chronic intestinal inflammation induced by 2,4,6,-trinitrobenzene sulfonic acid (TNBS) is characterized by a transmural granulomatous colitis that mimics some characteristics of human Crohn's disease. Here, we show that the transcription factor NF-kappa B p65 was strongly activated in TNBS-induced colitis and in colitis of interleukin-10-deficient mice. Local administration of p65 antisense phosphorothioate oligonucleotides abrogated clinical and histological signs of colitis and was more effective in treating TNBS-induced colitis than single or daily administration of glucocorticoids. The data provide direct evidence for the central importance of p65 in chronic intestinal inflammation and …

AdultMaleProtein subunitMolecular Sequence DataGeneral Biochemistry Genetics and Molecular BiologyMiceCrohn DiseaseAdrenal Cortex HormonesmedicineAnimalsHumansColitisTranscription factorCells CulturedAgedEnterocolitisPhosphorothioate OligonucleotidesBase Sequencebusiness.industryOligonucleotideEnterocolitisNF-kappa BTranscription Factor RelAGeneral MedicineDNAMiddle AgedOligonucleotides Antisensemedicine.diseaseNFKB1digestive system diseasesInterleukin-10Interleukin 10Disease Models AnimalTrinitrobenzenesulfonic AcidImmunologyCancer researchCytokinesFemalemedicine.symptombusinessNature medicine
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The atypical cannabinoid O-1602 protects against experimental colitis and inhibits neutrophil recruitment.

2011

Background: Cannabinoids are known to reduce intestinal inflammation. Atypical cannabinoids produce pharmacological effects via unidentified targets. We were interested in whether the atypical cannabinoid O-1602, reportedly an agonist of the putative cannabinoid receptor GPR55, reduces disease severity of dextran sulfate sodium (DSS) and trinitrobenzene sulfonic acid (TNBS)-induced colitis in C57BL/6N and CD1 mice. Methods: DSS (2.5% and 4%) was supplied in drinking water for 1 week while TNBS (4 mg) was applied as a single intrarectal bolus. Results: Both treatments caused severe colitis. Injection of O-1602 (5 mg/kg intraperitoneally) significantly reduced macroscopic and histological col…

AgonistMaleCannabinoid receptormedicine.drug_classColonNeutrophilsmedicine.medical_treatmentPharmacologyMotor ActivityInflammatory bowel diseaseArticleReceptors G-Protein-CoupledReceptor Cannabinoid CB2chemistry.chemical_compoundMiceReceptor Cannabinoid CB1CyclohexanesmedicineImmunology and AllergyAnimalsCannabidiolColitisReceptorReceptors CannabinoidPeroxidaseMice KnockoutAnalysis of VarianceO-1602business.industryCannabinoidsDextran SulfateGastroenterologyResorcinolsmedicine.diseaseColitisMice Inbred C57BLChemotaxis LeukocyteDisease Models AnimalchemistryGPR55Neutrophil InfiltrationTrinitrobenzenesulfonic AcidImmunologylipids (amino acids peptides and proteins)CannabinoidbusinessInflammatory bowel diseases
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Blood flow patterns spatially associated with platelet aggregates in murine colitis.

2009

In the normal murine mucosal plexus, blood flow is generally smooth and continuous. In inflammatory conditions, such as chemically-induced murine colitis, the mucosal plexus demonstrates markedly abnormal flow patterns. The inflamed mucosal plexus is associated with widely variable blood flow velocity as well as discontinuous and even bidirectional flow. To investigate the mechanisms responsible for these blood flow patterns, we used intravital microscopic examination of blood flow within the murine mucosal plexus during dextran sodium sulphate-and trinitrobenzenesulfonic acid-induced colitis. The blood flow patterns within the mucosal plexus demonstrated flow exclusion in 18% of the vessel…

Blood PlateletsPathologymedicine.medical_specialtyHistologyPlatelet AggregationInterleukin-1betaBiologyArticleMicrocirculationchemistry.chemical_compoundMiceIntestinal mucosamedicineAnimalsPlateletColitisIntestinal MucosaEcology Evolution Behavior and SystematicsPlexusMice Inbred BALB CGene Expression ProfilingMicrocirculationDextran SulfateBlood flowmedicine.diseaseColitisMice Inbred C57BLDextranchemistryTrinitrobenzenesulfonic AcidRegional Blood FlowAcute DiseaseEndothelium VascularAnatomyChemokinesIntravital microscopyBiotechnologyAnatomical record (Hoboken, N.J. : 2007)
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Low zone tolerance induced by systemic application of allergens inhibits TC1-mediated skin inflammation

2005

Background The induction of tolerance may be a promising target of strategies aimed at preventing harmful allergic diseases. Low zone tolerance (LZT), induced by epicutaneous application of low doses of contact allergens, inhibits the development of T C 1-mediated contact hypersensitivity (CHS). Objective We evaluated the effect of systemic (oral, intravenous) administration of low amounts of haptens on specific immune reactions and tolerance induction. Methods By using the mouse model of LZT, we analyzed immune reactions in vivo (skin inflammation) and T-cell responses in vitro after oral, intravenous, or epicutaneous application of low amounts of the contact allergen 2,4,6-trinitro-1-chlo…

CD4-Positive T-LymphocytesAdoptive cell transferAllergymedicine.medical_treatmentImmunologyDose-Response Relationship ImmunologicAdministration OralInflammationPicryl ChlorideAdministration CutaneousDermatitis ContactT-Lymphocytes RegulatoryImmune toleranceMiceImmune systemImmune TolerancemedicineAnimalsImmunology and AllergyMice KnockoutChemistryCell DifferentiationImmunotherapyAllergensmedicine.diseaseMice Inbred C57BLTolerance inductionTrinitrobenzenesulfonic AcidOrgan SpecificityInjections IntravenousImmunologymedicine.symptomCD8T-Lymphocytes CytotoxicJournal of Allergy and Clinical Immunology
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The flesh ethanolic extract of Hylocereus polyrhizus exerts anti-inflammatory effects and prevents murine colitis

2015

IBD is a chronic disorder of the gastrointestinal tract characterized by mucosal inflammation and epithelial damage. Biologic therapy has significantly improved the course of the disease but there are still a high percentage of patients that do not respond to current therapies. We aim to determine the effects of the flesh ethanolic extract of Hylocereus polyrhizus (EH) in a mice model of colitis induced by TNBS.Balb/c mice received TNBS (175 mg/kg, 100 μl, i.r.) and six and thirty hours later were administered with EH (1 g/kg, i.p.). Mice were weighted daily and after sacrificing (2 and 4 days after TNBS) we analyzed mucosal histology, myeloperoxidase activity (MPO), the expression of pro-i…

Cactaceae0301 basic medicineColonmedicine.drug_classAnti-Inflammatory AgentsGene ExpressionInflammationPharmacologyCritical Care and Intensive Care MedicineInflammatory bowel diseaseAnti-inflammatorylaw.inventionIrritable Bowel SyndromeMice03 medical and health sciences0404 agricultural biotechnologylawmedicineAnimalsColitisFlavonoidsMice Inbred BALB CGastrointestinal tractNutrition and DieteticsEthanolbiologyPlant Extractsbusiness.industryPolyphenols04 agricultural and veterinary sciencesColitismedicine.disease040401 food sciencedigestive system diseasesDisease Models Animal030104 developmental biologyTrinitrobenzenesulfonic AcidFruitMyeloperoxidaseImmunologySystemic administrationbiology.proteinCytokinesmedicine.symptomPhytotherapybusinessPhytotherapyClinical Nutrition
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Tolerance towards resident intestinal flora in mice is abrogated in experimental colitis and restored by treatment with interleukin-10 or antibodies …

1996

There is now increasing evidence that hyperresponsiveness towards intestinal flora is a crucial event in the pathogenesis of inflammatory bowel disease (IBD). In support of this hypothesis, we recently described in humans that tolerance exists towards indigenous intestinal flora but is broken in active IBD lesions. In the present study, we have attempted to transfer this model into mice from different genetic backgrounds (BALB/c, SJL/J, C3H/HeJ). We found that mononuclear cells from spleen, small bowel and large bowel of mice do not proliferate, i.e. are tolerant when exposed to bacterial sonicates derived from autologous intestine (BsA) but do proliferate, i.e. are immune when exposed to b…

ColonImmunologySpleenBiologyLymphocyte ActivationInflammatory bowel diseaseMicrobiologyMicePeyer's PatchesImmune systemCrohn DiseaseSpecies SpecificityImmunityIntestine SmallImmune TolerancemedicineAnimalsHumansImmunologic FactorsImmunology and AllergyColitisMice Inbred BALB CMice Inbred C3HBacteriaAntibodies MonoclonalInterleukinColitismedicine.diseaseInterleukin-12Recombinant ProteinsInterleukin-10RatsSpecific Pathogen-Free OrganismsIntestinesDisease Models AnimalInterleukin 10medicine.anatomical_structureTrinitrobenzenesulfonic AcidImmunologyLeukocytes MononuclearInterleukin 12SpleenEuropean Journal of Immunology
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