Search results for "Neutrophil Infiltration"

showing 10 items of 26 documents

Antagonization of IL-17A Attenuates Skin Inflammation and Vascular Dysfunction in Mouse Models of Psoriasis

2019

Besides skin inflammation, patients with severe psoriasis suffer from an increased risk of cardiovascular mortality. IL-17A plays a central role in the development of psoriasis and might connect skin and vascular disease. The aim of this study was to clarify whether anti-IL-17A therapy could also ameliorate the vascular dysfunction associated with severe psoriasis. We analyzed three murine models with varying severities of psoriasis-like skin disease concerning their vascular function and inflammation: (i) K14-IL-17A(ind/+) mice with keratinocyte-specific IL-17A overexpression and an early-onset severe psoriasis-like phenotype; (ii) homozygous CD11c-IL-17A(ind/ind) and heterozygous CD11c-IL…

0301 basic medicineInflammationDermatologyDiseasemedicine.disease_causeBiochemistryProinflammatory cytokine03 medical and health sciencesMice0302 clinical medicinePsoriasis Area and Severity IndexPsoriasismedicineAnimalsHumansPsoriasisVascular DiseasesAntibodies BlockingMolecular BiologyAortaSkinInflammationImiquimodintegumentary systembusiness.industryVascular diseaseInterleukin-17Cell Biologymedicine.diseaseAngiotensin II3. Good healthMice Inbred C57BLDisease Models AnimalOxidative Stress030104 developmental biologyNeutrophil Infiltration030220 oncology & carcinogenesisImmunologyDisease Progression[SDV.IMM]Life Sciences [q-bio]/ImmunologyImmunotherapymedicine.symptombusinessReactive Oxygen SpeciesOxidative stress
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Loss of cellular FLICE-inhibitory protein promotes acute cholestatic liver injury and inflammation from bile duct ligation.

2017

Cholestatic liver injury results from impaired bile flow or metabolism and promotes hepatic inflammation and fibrogenesis. Toxic bile acids that accumulate in cholestasis induce apoptosis and contribute to early cholestatic liver injury, which is amplified by accompanying inflammation. The aim of the current study was to evaluate the role of the antiapoptotic caspase 8-homolog cellular FLICE-inhibitory (cFLIP) protein during acute cholestatic liver injury. Transgenic mice exhibiting hepatocyte-specific deletion of cFLIP (cFLIP−/−) were used for in vivo and in vitro analysis of cholestatic liver injury using bile duct ligation (BDL) and the addition of bile acids ex vivo. Loss of cFLIP in h…

0301 basic medicineLiver CirrhosisTime FactorsPhysiologyCASP8 and FADD-Like Apoptosis Regulating ProteinInflammationApoptosisp38 Mitogen-Activated Protein KinasesHepatitisBile Acids and Salts03 medical and health sciencesNecrosisCholestasisPhysiology (medical)medicineHepatic Stellate CellsAnimalsASK1Genetic Predisposition to DiseaseLigationCells CulturedTumor Necrosis Factor alpha-Induced Protein 3chemistry.chemical_classificationLiver injuryCommon Bile DuctMice KnockoutReactive oxygen speciesHepatologyBile duct ligationGastroenterologyTranscription Factor RelAmedicine.diseaseOxidative Stress030104 developmental biologyCholedocholithiasisPhenotypechemistryLiverNeutrophil InfiltrationApoptosisFLICE Inhibitory ProteinCancer researchHepatocytesCytokinesmedicine.symptomInflammation MediatorsSignal TransductionAmerican journal of physiology. Gastrointestinal and liver physiology
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Gut Microbiota Restricts NETosis in Acute Mesenteric Ischemia-Reperfusion Injury.

2020

Objective: Recruitment of neutrophils and formation of neutrophil extracellular traps (NETs) contribute to lethality in acute mesenteric infarction. To study the impact of the gut microbiota in acute mesenteric infarction, we used gnotobiotic mouse models to investigate whether gut commensals prime the reactivity of neutrophils towards formation of neutrophil extracellular traps (NETosis). Approach and Results: We applied a mesenteric ischemia-reperfusion (I/R) injury model to germ-free (GF) and colonized C57BL/6J mice. By intravital imaging, we quantified leukocyte adherence and NET formation in I/R-injured mesenteric venules. Colonization with gut microbiota or monocolonization with Esch…

0301 basic medicineMaleExtracellular TrapsMesenteric infarctionLipopolysaccharideNeutrophilsGut floraExtracellular Traps03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAcute mesenteric ischemiaVenulesmedicineCell AdhesionEscherichia coliLeukocytesAnimalsGerm-Free LifeLeukocyte RollingMesenteryCells CulturedMice Knockoutbiologybusiness.industryNeutrophil extracellular trapsbiology.organism_classificationmedicine.diseaseGastrointestinal MicrobiomeMice Inbred C57BLToll-Like Receptor 4Disease Models Animal030104 developmental biologychemistryNeutrophil Infiltration030220 oncology & carcinogenesisMesenteric IschemiaReperfusion InjuryImmunologyHost-Pathogen InteractionsFemaleCardiology and Cardiovascular MedicinebusinessReperfusion injuryBacillus subtilisSignal TransductionArteriosclerosis, thrombosis, and vascular biology
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Pleural Mesothelial Cells Express Both BLT2 and PPARα and Mount an Integrated Response to Pleural Leukotriene B4

2008

Abstract Leukotriene B4 (LTB4) plays a crucial role in the recruitment of neutrophils into the pleural space. We identified for the first time the mechanisms by which LTB4 interacts with mesothelial cells and recruits neutrophils in the pleural compartment. Primary pleural mesothelial cells express both the proinflammatory receptor for LTB4 BLT2, and the anti-inflammatory receptor for LTB4, PPARα. Parapneumonic pleural effusions highly increase BLT2 expression and, via BLT2 activation, increase the adhesion between mesothelial cells and neutrophils and the expression of ICAM-1 on mesothelial cells. The block of PPARα further increases both cell adhesion and ICAM-1 expression. BLT2 activatio…

Adultmedicine.drug_classLeukotriene B4Blotting WesternImmunologyReceptors Leukotriene B4Protein tyrosine phosphataseBiologyLeukotriene B4EpitheliumTyrosine-kinase inhibitorProinflammatory cytokinechemistry.chemical_compoundCell AdhesionmedicineHumansImmunology and AllergyPPAR alphaCell adhesionCells CulturedAgedInflammationLeukotriene B4 receptorPneumoniaMiddle Agedrespiratory systemFlow CytometryIntercellular Adhesion Molecule-1respiratory tract diseasesPleural EffusionChemotaxis LeukocyteNeutrophil InfiltrationchemistryImmunologyCancer researchPleuraPhosphorylationMesothelial CellThe Journal of Immunology
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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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An Alternative Pathway of Imiquimod-Induced Psoriasis-Like Skin Inflammation in the Absence of Interleukin-17 Receptor A Signaling

2013

Topical application of imiquimod (IMQ) on the skin of mice induces inflammation with common features found in psoriatic skin. Recently, it was postulated that IL-17 has an important role both in psoriasis and in the IMQ model. To further investigate the impact of IL-17RA signaling in psoriasis, we generated IL-17 receptor A (IL-17RA)-deficient mice (IL-17RA(del)) and challenged these mice with IMQ. Interestingly, the disease was only partially reduced and delayed but not abolished when compared with controls. In the absence of IL-17RA, we found persisting signs of inflammation such as neutrophil and macrophage infiltration within the skin. Surprisingly, already in the naive state, the skin …

ChemokineInflammationImiquimodDermatologyInterleukin-17 receptorBiochemistryMiceAdjuvants ImmunologicPsoriasismedicineAnimalsPsoriasisMacrophageMolecular BiologySkinMice KnockoutImiquimodReceptors Interleukin-17biologyInterleukin-6InterleukinsMacrophagesInterleukin-17Cell Biologymedicine.diseaseDisease Models AnimalCXCL2Neutrophil InfiltrationImmunologyAminoquinolinesbiology.proteinFemaleTumor necrosis factor alphamedicine.symptomSignal Transductionmedicine.drugJournal of Investigative Dermatology
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Impairment of TGF-β signaling in T cells increases susceptibility to experimental autoimmune hepatitis in mice

2002

In autoimmune hepatitis, strong TGF-beta1 expression is found in the inflamed liver. TGF-beta overexpression may be part of a regulatory immune response attempting to suppress autoreactive T cells. To test this hypothesis, we determined whether impairment of TGF-beta signaling in T cells leads to increased susceptibility to experimental autoimmune hepatitis (EAH). Transgenic mice of strain FVB/N were generated expressing a dominant-negative TGF-beta type II receptor in T cells under the control of the human CD2 promoter/locus control region. On induction of EAH, transgenic mice showed markedly increased portal and periportal leukocytic infiltrations with hepatocellular necroses compared wit…

Genetically modified mouseCellular immunityPhysiologyT-LymphocytesEnzyme-Linked Immunosorbent AssayMice TransgenicAutoimmune hepatitisBiologyMiceImmune systemTransforming Growth Factor betaPhysiology (medical)medicineAnimalsHomeostasisCells CulturedAutoimmune diseaseHepatitisB-LymphocytesHepatologyGastroenterologyT lymphocyteBlotting Northernmedicine.diseaseImmunohistochemistryHepatitis AutoimmunePhenotypeNeutrophil InfiltrationImmunologySignal transductionSignal TransductionAmerican Journal of Physiology-Gastrointestinal and Liver Physiology
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Timing effect of intramyocardial hydrogel injection for positively impacting left ventricular remodeling after myocardial infarction

2015

Intramyocardial injection of various injectable hydrogel materials has shown benefit in positively impacting the course of left ventricular (LV) remodeling after myocardial infarction (MI). However, since LV remodeling is a complex, time dependent process, the most efficacious time of hydrogel injection is not clear. In this study, we injected a relatively stiff, thermoresponsive and bioabsorbable hydrogel in rat hearts at 3 different time points - immediately after MI (IM), 3 d post-MI (3D), and 2 w post-MI (2W), corresponding to the beginnings of the necrotic, fibrotic and chronic remodeling phases. The employed left anterior descending coronary artery ligation model showed expected infar…

InjectionTime FactorsMacrophageMyocardial InfarctionInfarction02 engineering and technology030204 cardiovascular system & hematologyCardiac tissue engineeringAntigens CD31Hydrogel Polyethylene Glycol DimethacrylateHeart Ventricle0302 clinical medicineFibrosisMyocardial infarctionInflammation MediatorVentricular RemodelingIntervention timing021001 nanoscience & nanotechnologyPlatelet Endothelial Cell Adhesion Molecule-1Neutrophil InfiltrationMechanics of MaterialsSelf-healing hydrogelsCardiologyCytokinesFemalemedicine.symptomInflammation Mediators0210 nano-technologymedicine.medical_specialtyMaterials scienceTime FactorHeart VentriclesBiophysicsInflammationBioengineeringCeramics and CompositeAnterior Descending Coronary ArteryArticleInjectionsBiomaterials03 medical and health sciencesInternal medicinemedicineAnimalsMechanics of MaterialVentricular remodelingCytokineActinAnimalMacrophagesMyocardiummedicine.diseaseBiomaterialInjectable materialActinsHydrogelRats Inbred LewCeramics and CompositesLigation
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Increased Susceptibility to Skin Carcinogenesis Associated with a Spontaneous Mouse Mutation in the Palmitoyl Transferase Zdhhc13 Gene

2015

International audience; Here we describe a spontaneous mutation in the Zdhhc13 (zinc finger, DHHC domain containing 13) gene (also called Hip14l), one of 24 genes encoding palmitoyl acyltransferase (PAT) enzymes in the mouse. This mutation (Zdhhc13luc) was identified as a nonsense base substitution, which results in a premature stop codon that generates a truncated form of the ZDHHC13 protein, representing a potential loss-of-function allele. Homozygous Zdhhc13luc/Zdhhc13luc mice developed generalized hypotrichosis, associated with abnormal hair cycle, epidermal and sebaceous gland hyperplasia, hyperkeratosis, and increased epidermal thickness. Increased keratinocyte proliferation and accel…

KeratinocytesPathologySkin NeoplasmsMutantMESH: Codon TerminatorMESH: Epidermal Cellsmedicine.disease_causeBiochemistryMESH: Acyltransferases / genetics*MESH: Keratinocytes / physiologyMice0302 clinical medicineHair cycleMESH: AnimalsPalmitoyl acyltransferase0303 health sciencesintegumentary systemNF-kappa B3. Good healthPhenotypemedicine.anatomical_structureNeutrophil Infiltration030220 oncology & carcinogenesisCodon TerminatorKeratinocytemedicine.medical_specialtyClinical SciencesOncology and CarcinogenesisDermatologyBiologyMESH: PhenotypeMESH: Skin Neoplasms / etiologyArticleMESH: Skin Neoplasms / genetics*03 medical and health sciencesMESH: Genetic Predisposition to Disease*medicineAnimalsGenetic Predisposition to DiseaseTerminatorMESH: NF-kappa B / physiologyCodonMESH: MiceMolecular Biology030304 developmental biologyEpidermis (botany)Dermatology & Venereal DiseasesMESH: Leukocyte Elastase / metabolismCell BiologyMESH: Bromodeoxyuridine / metabolismNFKB1Molecular biologyMESH: Neutrophil Infiltration[SDV.GEN.GA]Life Sciences [q-bio]/Genetics/Animal geneticsBromodeoxyuridineEpidermal CellsMutationNIH 3T3 CellsMESH: Mutation*Leukocyte ElastaseCarcinogenesisDHHC domainAcyltransferasesMESH: NIH 3T3 CellsJournal of Investigative Dermatology
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Mast Cell Deficiency Protects Susceptible BALB/c Mice from Progressive Murine Cutaneous Leishmaniasis.

2020

Leishmaniasis CutaneousMice TransgenicDermatologyBiochemistryBALB/cMiceCutaneous leishmaniasismedicineAnimalsHumansMast CellsMolecular BiologyLeishmania majorMice Inbred BALB CbiologyCell Biologymedicine.diseasebiology.organism_classificationMast cellDisease Models AnimalProto-Oncogene Proteins c-kitmedicine.anatomical_structureNeutrophil InfiltrationImmunologyTh17 CellsDisease SusceptibilityThe Journal of investigative dermatology
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