2024
Ezrin drives adaptation of monocytes to the inflamed lung microenvironment
Gudneppanavar R, Di Pietro C, H Öz H, Zhang P, Cheng E, Huang P, Tebaldi T, Biancon G, Halene S, Hoppe A, Kim C, Gonzalez A, Krause D, Egan M, Gupta N, Murray T, Bruscia E. Ezrin drives adaptation of monocytes to the inflamed lung microenvironment. Cell Death & Disease 2024, 15: 864. PMID: 39613751, PMCID: PMC11607083, DOI: 10.1038/s41419-024-07255-8.Peer-Reviewed Original ResearchConceptsActivation of focal adhesion kinaseExtracellular matrixActin-binding proteinsFocal adhesion kinaseLung extracellular matrixKnock-out mouse modelProtein kinase signalingCortical cytoskeletonLoss of ezrinKinase signalingPlasma membraneCell migrationSignaling pathwayEzrinResponse to lipopolysaccharideTissue-resident macrophagesMouse modelLipopolysaccharideCytoskeletonEzrin expressionLung microenvironmentKinaseMonocyte recruitmentProteinAktCaspase-4/11 promotes hyperlipidemia and chronic kidney disease-accelerated vascular inflammation by enhancing trained immunity
Sun Y, Lu Y, Liu L, Saaoud F, Shao Y, Xu K, Drummer C, Cueto R, Shan H, Jiang X, Zhao H, Wang H, Yang X. Caspase-4/11 promotes hyperlipidemia and chronic kidney disease-accelerated vascular inflammation by enhancing trained immunity. JCI Insight 2024, 9: e177229. PMID: 39024553, PMCID: PMC11343595, DOI: 10.1172/jci.insight.177229.Peer-Reviewed Original ResearchChronic kidney diseaseTrained immunityAortic endothelial cellsVascular inflammationEndothelial cellsRecruitment of macrophagesIL-1b levelsHuman aortic endothelial cellsHigh-fat dietMembrane expressionN-terminal gasdermin DCytokine secretionPathological analysisIL-1BKidney diseaseNeointima hyperplasiaCaspase-4/11HyperlipidemiaInflammationCytosolic lipopolysaccharideCaspase-11RNA sequencingGasdermin DImmunityLipopolysaccharide
2022
Serological and molecular epidemiology of leptospirosis and the role of dogs as sentinel for human infection in Nigeria
Pilau NN, Lubar AA, Daneji AI, Mera UM, Magaji AA, Abiayi EA, Chaiboonma KL, Busayo EI, Vinetz JM, Matthias MA. Serological and molecular epidemiology of leptospirosis and the role of dogs as sentinel for human infection in Nigeria. Heliyon 2022, 8: e09484. PMID: 35647333, PMCID: PMC9136256, DOI: 10.1016/j.heliyon.2022.e09484.Peer-Reviewed Original ResearchProspective cross-sectional studyCarriers of leptospiresCross-sectional studySymptomatic dogsQuantitative real-time PCRRole of dogsBacteriological prevalenceReal-time PCRUnvaccinated animalsHigh riskLeptospiral infectionInfection rateHuman infectionsPublic health riskMolecular epidemiologyStray dogsInfectionDogsCulture isolationO-antigen regionHealth risksLeptospirosisLipopolysaccharideSerogroupsStrong determinantIntrinsic cardiac adrenergic cells contribute to LPS-induced myocardial dysfunction
Yang D, Dai X, Xing Y, Tang X, Yang G, Harrison A, Cahoon J, Li H, Lv X, Yu X, Wang P, Wang H. Intrinsic cardiac adrenergic cells contribute to LPS-induced myocardial dysfunction. Communications Biology 2022, 5: 96. PMID: 35079095, PMCID: PMC8789803, DOI: 10.1038/s42003-022-03007-6.Peer-Reviewed Original ResearchConceptsIntrinsic cardiac adrenergic cellsToll-like receptor 4ICA cellsTNF-α productionMyocardial dysfunctionSeptic cardiomyopathyAdrenergic cellsMyocardial TNF-α productionSecretion of NEPotential therapeutic targetΒ1-adrenergic receptorNE biosynthesisTLR4-MyD88Receptor 4Norepinephrine secretionP65 translocationTyrosine hydroxylaseNF-κBTherapeutic targetMitogen-activated protein kinase pathwayDependent protein kinase IILipopolysaccharideDysfunctionProtein kinase IIPathological processes
2020
Late Breaking Abstract - The airway sensory nerve transcriptome: evidence for neuropathic injury following lipopolysaccharide induced lung inflammation
Caceres A, Kaelberer M, Jordt S. Late Breaking Abstract - The airway sensory nerve transcriptome: evidence for neuropathic injury following lipopolysaccharide induced lung inflammation. 2020, 902. DOI: 10.1183/13993003.congress-2020.902.Peer-Reviewed Original ResearchPseudomonas aeruginosa Utilizes Host-Derived Itaconate to Redirect Its Metabolism to Promote Biofilm Formation
Riquelme SA, Liimatta K, Wong Fok Lung T, Fields B, Ahn D, Chen D, Lozano C, Sáenz Y, Uhlemann AC, Kahl BC, Britto CJ, DiMango E, Prince A. Pseudomonas aeruginosa Utilizes Host-Derived Itaconate to Redirect Its Metabolism to Promote Biofilm Formation. Cell Metabolism 2020, 31: 1091-1106.e6. PMID: 32428444, PMCID: PMC7272298, DOI: 10.1016/j.cmet.2020.04.017.Peer-Reviewed Original ResearchConceptsHost immune responseImmune responseDownregulation of lipopolysaccharidesIntractable pneumoniaPseudomonas aeruginosaInfected lungsChronic infectionImmune clearanceHuman airwaysImmunostimulatory propertiesMyeloid cellsHigh mortalityAirwayInfectionOpportunistic bacteriaLipopolysaccharideAeruginosaBiofilm formationResponsePneumoniaLungTherapyMortalityClearanceUpregulation
2018
Lipopolysaccharide stimulates BK channel activity in bladder umbrella cells
Lu M, Li JR, Alvarez-Lugo L, Li Y, Yu S, Li X, Shi B, Chai TC. Lipopolysaccharide stimulates BK channel activity in bladder umbrella cells. American Journal Of Physiology - Cell Physiology 2018, 314: c643-c653. PMID: 29466671, DOI: 10.1152/ajpcell.00339.2017.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCyclic AMP-Dependent Protein KinasesFemaleLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsLipopolysaccharide ReceptorsLipopolysaccharidesLymphocyte Antigen 96Membrane PotentialsMice, Inbred C57BLPatch-Clamp TechniquesPotassiumSignal TransductionToll-Like Receptor 4Urinary BladderUrinary Tract InfectionsUrotheliumConceptsBK channel activityBK channelsChannel activityUmbrella cellsUrinary tract infectionFemale C57BL6 micePotassium channel inhibitorsUropathogenic Escherichia coliProtein kinase ATract infectionsLPS effectsC57BL6 miceBladder urotheliumLamina propriaMin of exposureChannel inhibitorsBacterial infectionsLPS receptorUrothelial tissuesUrothelial cellsUrotheliumLipopolysaccharidePotassium channelsRT-PCRPKA blocker
2017
MP82-07 UROTHELIAL GENES MODULATING MICTURITION BEHAVIOR INDUCED BY A REPETITIVE LIPOPOLYSACCHARIDE (LPS) EXPOSURE IN AN OVARIECTOMIZED (OVX) MOUSE MODEL
Acevedo-Alvarez M, Yeh J, Alvarez-Lugo L, Lu M, Sukumar N, Hill W, Chai T. MP82-07 UROTHELIAL GENES MODULATING MICTURITION BEHAVIOR INDUCED BY A REPETITIVE LIPOPOLYSACCHARIDE (LPS) EXPOSURE IN AN OVARIECTOMIZED (OVX) MOUSE MODEL. Journal Of Urology 2017, 197: e1099. DOI: 10.1016/j.juro.2017.02.2554.Peer-Reviewed Original ResearchPD12-05 BIG POTASSIUM CHANNEL (BK) ACTIVITY IN FEMALE MOUSE BLADDER UMBRELLA CELLS IS ENHANCED BY BACTERIAL LIPOPOLYSACCHARIDE: AN ACUTE HOST RESPONSE IN URINARY TRACT INFECTION (UTI) PATHOGENESIS
Lu M, Li J, Li Y, Yu S, Chai T. PD12-05 BIG POTASSIUM CHANNEL (BK) ACTIVITY IN FEMALE MOUSE BLADDER UMBRELLA CELLS IS ENHANCED BY BACTERIAL LIPOPOLYSACCHARIDE: AN ACUTE HOST RESPONSE IN URINARY TRACT INFECTION (UTI) PATHOGENESIS. Journal Of Urology 2017, 197: e267. DOI: 10.1016/j.juro.2017.02.680.Peer-Reviewed Original Research
2016
Chromium alters lipopolysaccharide-induced inflammatory responses both in vivo and in vitro
Jin Y, Liu L, Zhang S, Tao B, Tao R, He X, Qu L, Huang J, Wang X, Fu Z. Chromium alters lipopolysaccharide-induced inflammatory responses both in vivo and in vitro. Chemosphere 2016, 148: 436-443. PMID: 26841286, DOI: 10.1016/j.chemosphere.2016.01.057.Peer-Reviewed Original ResearchConceptsInducible nitric oxide synthaseInterleukin-6Inflammatory responseCyclooxygenase-2 mRNA levelsLipopolysaccharide-induced inflammatory responsesRelease of TNFαNitric oxide synthaseTumor necrosis factorCell linesRAW264.7 cell lineConcentration-dependent mannerSerum levelsInflammatory cellsInterleukin-1βLiver weightOxide synthaseMacrophage cell lineNecrosis factorInterleukin-1αCR pretreatmentCytokine genesPeritoneal macrophagesSerious infiltrationLipopolysaccharideMRNA levels
2013
Adenosine is required for sustained inflammasome activation via the A2A receptor and the HIF-1α pathway
Ouyang X, Ghani A, Malik A, Wilder T, Colegio OR, Flavell RA, Cronstein BN, Mehal WZ. Adenosine is required for sustained inflammasome activation via the A2A receptor and the HIF-1α pathway. Nature Communications 2013, 4: 2909. PMID: 24352507, PMCID: PMC3895487, DOI: 10.1038/ncomms3909.Peer-Reviewed Original ResearchMeSH KeywordsAdenosineAdenosine TriphosphateAnimalsCarrier ProteinsCyclic AMPCyclic AMP Response Element-Binding ProteinCyclic AMP-Dependent Protein KinasesHypoxia-Inducible Factor 1, alpha SubunitInflammasomesInterleukin-1betaLipopolysaccharidesLiverMacrophagesMaleMiceMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinReceptor, Adenosine A2ASignal TransductionConceptsHIF-1α pathwayInflammasome activityInflammasome activationA2A receptorsIL-1β productionIL-1β responseReceptor-mediated signalingLack of responseTolerogenic stateChronic diseasesInflammatory responseInflammasome pathwayPrevious exposureLipopolysaccharideAdenosineReceptorsActivationKey regulatorInitial activationPathwaySignalingResponseInterleukinStimuliDisease
2012
Lipopolysaccharide Appears to Activate Human Endometrial Endothelial Cells Through TLR‐4‐Dependent and TLR‐4‐Independent Mechanisms
Krikun G, Trezza J, Shaw J, Rahman M, Guller S, Abrahams VM, Lockwood CJ. Lipopolysaccharide Appears to Activate Human Endometrial Endothelial Cells Through TLR‐4‐Dependent and TLR‐4‐Independent Mechanisms. American Journal Of Reproductive Immunology 2012, 68: 233-237. PMID: 22672000, PMCID: PMC3418410, DOI: 10.1111/j.1600-0897.2012.01164.x.Peer-Reviewed Original ResearchConceptsEndometrial endothelial cellsTissue factor expressionHuman endometrial endothelial cellsToll-like receptorsLPS-RSFactor expressionEndothelial cellsBacterial lipopolysaccharideTLR-4Innate immunityCytokine/chemokine responsesTLR-4 antagonistGram-negative bacterial lipopolysaccharideChemokine responsesIL-6IL-8Cytokine secretionG-CSFWestern blotLipopolysaccharideBacterial componentsCell-free supernatantMD-2ImmunitySecretion
2011
Modulation of Amniotic Fluid Activin‐A and Inhibin‐A in Women With Preterm Premature Rupture of the Membranes and Infection‐Induced Preterm Birth
Rosenberg VA, Buhimschi IA, Dulay AT, Abdel‐Razeq S, Oliver EA, Duzyj CM, Lipkind H, Pettker CM, Buhimschi CS. Modulation of Amniotic Fluid Activin‐A and Inhibin‐A in Women With Preterm Premature Rupture of the Membranes and Infection‐Induced Preterm Birth. American Journal Of Reproductive Immunology 2011, 67: 122-131. PMID: 21992678, PMCID: PMC3253234, DOI: 10.1111/j.1600-0897.2011.01074.x.Peer-Reviewed Original ResearchConceptsPreterm premature rupturePreterm birthPremature ruptureVillous explantsRecombinant activinInflammation-induced preterm birthRelease of activinIntra-amniotic infectionPlacental villous explantsIL-8 releasePreterm laborInflammatory processInflammatory reactionGram-negative lipopolysaccharideInhibinFetal membranesHuman AFImportant modulatorAF samplesInfectionActivinLipopolysaccharidePPROMAmniochorionIntact membranes
2009
Inflammasome-activating biodegradable nanoparticulates as vaccine delivery systems (135.80)
Fahmy T, DEMENTO S, Eisenbarth S, Caplan M, Saltzman W, Mellman I, Ledizet M, Fikrig E, Flavell R. Inflammasome-activating biodegradable nanoparticulates as vaccine delivery systems (135.80). The Journal Of Immunology 2009, 182: 135.80-135.80. DOI: 10.4049/jimmunol.182.supp.135.80.Peer-Reviewed Original ResearchToll-like receptorsIL-1βInflammasome activationProinflammatory cytokines IL-1βAntigen-presenting cellsClass of nanomaterialsCytokines IL-1βSurface of nanoparticlesWest Nile encephalitisInnate immune pathwaysVaccine delivery systemWild-type macrophagesCellular immunityVaccination approachesMurine modelInflammasome activityType macrophagesImmune pathwaysAdjuvant deliveryDanger signalsVaccine designModel antigenLipopolysaccharideAntigenBiocompatible polyesterORIGINAL ARTICLE: Regulation of Nod1 and Nod2 in First Trimester Trophoblast Cells
Mulla MJ, Yu AG, Cardenas I, Guller S, Panda B, Abrahams VM. ORIGINAL ARTICLE: Regulation of Nod1 and Nod2 in First Trimester Trophoblast Cells. American Journal Of Reproductive Immunology 2009, 61: 294-302. PMID: 19260860, DOI: 10.1111/j.1600-0897.2009.00694.x.Peer-Reviewed Original ResearchMeSH KeywordsApoptosisBenzamidesCells, CulturedCytokinesDiaminopimelic AcidFemaleGene Expression Regulation, DevelopmentalHumansLipopolysaccharidesNF-kappa BNod1 Signaling Adaptor ProteinNod2 Signaling Adaptor ProteinPregnancyPregnancy Trimester, FirstSequence DeletionSignal TransductionThiazolesToll-Like Receptor 4TransgenesTrophoblastsConceptsFirst trimester trophoblast cellsTrophoblast cellsExpression of NOD1Cytoplasmic pattern recognition receptorsProduction of cytokinesNOD2 mRNA expressionPattern recognition receptorsNOD2 expressionCytokine responsesInflammatory responseNOD2 activationNOD1 activationNFkappaB inhibitorRecognition receptorsNOD1Nod1 stimulationNOD2Bacterial lipopolysaccharideMRNA expressionTLR4LipopolysaccharideNFkappaB pathwayRT-PCRBacterial peptidesTrophoblast
2006
The expression and function of enterocyte toll like receptor-4 are enhanced by lipopolysaccharide in vitro and during systemic endotoxemia
Cavallo J, Leaphart C, Li-Korotky H, Lo C, Li J, Hackam D. The expression and function of enterocyte toll like receptor-4 are enhanced by lipopolysaccharide in vitro and during systemic endotoxemia. Journal Of Surgical Research 2006, 130: 232. DOI: 10.1016/j.jss.2005.11.198.Peer-Reviewed Original Research
2001
Development of chronic colitis is dependent on the cytokine MIF
de Jong Y, Abadia-Molina A, Satoskar A, Clarke K, Rietdijk S, Faubion W, Mizoguchi E, Metz C, Sahli M, ten Hove T, Keates A, Lubetsky J, Farrell R, Michetti P, van Deventer S, Lolis E, David J, Bhan A, Terhorst C. Development of chronic colitis is dependent on the cytokine MIF. Nature Immunology 2001, 2: 1061-1066. PMID: 11668338, DOI: 10.1038/ni720.Peer-Reviewed Original ResearchMeSH KeywordsAdoptive TransferAnimalsAutoimmune DiseasesBone Marrow TransplantationChronic DiseaseColitisCrohn DiseaseDNA-Binding ProteinsFemaleHumansImmunization, PassiveLipopolysaccharidesMacrophage ActivationMacrophage Migration-Inhibitory FactorsMaleMiceMice, KnockoutModels, AnimalNuclear ProteinsRadiation ChimeraWeight LossConceptsMacrophage migration inhibitory factorCytokine macrophage migration inhibitory factorMIF-deficient miceCrohn's diseaseRole of MIFImmune systemPlasma MIF concentrationMucosal immune systemInnate immune cellsInnate immune systemChronic colitisMIF concentrationsExperimental colitisMIF productionMurine colitisImmune cellsColitisIntestinal bacteriaInhibitory factorDiseaseNew targetsMiceLipopolysaccharideCell typesPatients
1998
Cyclooxygenase Expression in Bovine Aortic Endothelial Cells Exposed to Cyclic Strain
Kito H, Yokoyama C, Inoue H, Tanabe T, Nakajima N, Sumpio B. Cyclooxygenase Expression in Bovine Aortic Endothelial Cells Exposed to Cyclic Strain. Endothelium 1998, 6: 107-112. PMID: 9930644, DOI: 10.3109/10623329809072197.Peer-Reviewed Original ResearchConceptsAortic endothelial cellsBovine aortic endothelial cellsEndothelial cellsInduction of COXCOX-1 expressionCOX-2 promoter activityExposure of ECsPromoter activityCycles/minCOX-2Cyclooxygenase expressionCOX-1Weak inducerMRNA expressionExtent of inductionNorthern blot analysisBlot analysisTransient transfection experimentsLipopolysaccharideMinimal effectExpressionInductionTransfection experimentsCyclic strainCells
1995
Altered responses to bacterial infection and endotoxic shock in mice lacking inducible nitric oxide synthase
MacMicking J, Nathan C, Hom G, Chartrain N, Fletcher D, Trumbauer M, Stevens K, Xie Q, Sokol K, Hutchinson N, Chen H, Mudget J. Altered responses to bacterial infection and endotoxic shock in mice lacking inducible nitric oxide synthase. Cell 1995, 81: 641-650. PMID: 7538909, DOI: 10.1016/0092-8674(95)90085-3.Peer-Reviewed Original ResearchConceptsInducible nitric oxide synthaseINOS-/- miceNitric oxide synthaseOxide synthaseAnesthetized wild-type miceCentral arterial blood pressureArterial blood pressureWild-type miceBacterial endotoxic lipopolysaccharidesBlood pressureLiver damagePropionobacterium acnesEarly deathInfectious agentsTissue damageBacterial infectionsTumor cellsLymphoma cellsLipopolysaccharideAltered responseMiceEndotoxic lipopolysaccharideDeathListeria monocytogenesHypotension
1989
Osteoblast-Like Cells Secrete Granulocyte-Macrophage Colony-Stimulating Factor in Response to Parathyroid Hormone and Lipopolysaccharide*
WEIR EC, INSOGNA KL, HOROWITZ MC. Osteoblast-Like Cells Secrete Granulocyte-Macrophage Colony-Stimulating Factor in Response to Parathyroid Hormone and Lipopolysaccharide*. Endocrinology 1989, 124: 899-904. PMID: 2643512, DOI: 10.1210/endo-124-2-899.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DivisionCell LineColony-Stimulating FactorsDNA ReplicationGranulocyte-Macrophage Colony-Stimulating FactorGrowth SubstancesInterleukin-2Interleukin-3Interleukin-4InterleukinsKineticsLipopolysaccharidesOsteoblastsOsteosarcomaParathyroid HormoneRatsRecombinant ProteinsThymidineConceptsGranulocyte-macrophage colony-stimulating factorInterleukin-2GM-CSF antibodyIL-4Colony-stimulating factorMitogenic activityCSF antibodiesROS cellsGM-CSFT-cell mitogenic activityPresence of antibodiesDose-dependent increaseHT-2 cellsBone resorptionOsteoblast-like cellsOsteoclast precursorsPTHCell CMLipopolysaccharideAntibodiesCellular mechanismsEffect of incubationCytokinesBiochemical criteriaCSF
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