2021
Macrophage-preferable delivery of the leucine-rich repeat domain of NLRX1 ameliorates lethal sepsis by regulating NF-κB and inflammasome signaling activation
Koo JH, Kim SH, Jeon SH, Kang MJ, Choi JM. Macrophage-preferable delivery of the leucine-rich repeat domain of NLRX1 ameliorates lethal sepsis by regulating NF-κB and inflammasome signaling activation. Biomaterials 2021, 274: 120845. PMID: 33971559, DOI: 10.1016/j.biomaterials.2021.120845.Peer-Reviewed Original ResearchConceptsSystemic inflammationSepsis modelNF-κBAcute systemic inflammatory diseaseSymptoms of sepsisSystemic inflammatory diseaseAnti-TNFα antibodyIL-6 productionIL-1β productionEffective therapeutic agentCaspase-1 activationOrgan dysfunctionLethal sepsisTreatment optionsInflammatory diseasesP65 phosphorylationSepsisIκB degradationBacterial infectionsPeritoneal macrophagesTherapeutic agentsMacrophagesInflammationInflammasomeLPS
2019
Syk-dependent glycolytic reprogramming in dendritic cells regulates IL-1β production to β-glucan ligands in a TLR-independent manner
Thwe PM, Fritz DI, Snyder JP, Smith PR, Curtis KD, O'Donnell A, Galasso NA, Sepaniac LA, Adamik BJ, Hoyt LR, Rodriguez PD, Hogan TC, Schmidt AF, Poynter ME, Amiel E. Syk-dependent glycolytic reprogramming in dendritic cells regulates IL-1β production to β-glucan ligands in a TLR-independent manner. Journal Of Leukocyte Biology 2019, 106: 1325-1335. PMID: 31509298, PMCID: PMC6883127, DOI: 10.1002/jlb.3a0819-207rr.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsbeta-GlucansDendritic CellsGlycolysisInterleukin-1betaLectins, C-TypeLigandsMiceMyeloid Differentiation Factor 88NLR Family, Pyrin Domain-Containing 3 ProteinPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktSignal TransductionSyk KinaseToll-Like ReceptorsConceptsTLR-independent mannerDendritic cellsGlucan ligandMetabolic regulationMetabolic reprogramming eventsGlycolytic reprogrammingPyrin domain-containing protein 3 (NLRP3) inflammasome activationActivation of DCsProtein 3 inflammasome activationC-type lectin receptorsImmune effector functionsReprogramming eventsIL-1β productionImmune cell activationInnate immune receptorsFungal microbesMetabolic reprogrammingTyrosine kinaseReprogrammingImmune receptorsCytokine productionIL-1βT cellsInflammasome activationEffector functions
2018
Role of NOD2 in antiphospholipid antibody-induced and bacterial MDP amplification of trophoblast inflammation
Mulla MJ, Pasternak MC, Salmon JE, Chamley LW, Abrahams VM. Role of NOD2 in antiphospholipid antibody-induced and bacterial MDP amplification of trophoblast inflammation. Journal Of Autoimmunity 2018, 98: 103-112. PMID: 30594350, DOI: 10.1016/j.jaut.2018.12.003.Peer-Reviewed Original ResearchConceptsMuramyl dipeptideAbsence of aPLAnti-angiogenic profileNovel danger signalPresence of aPLRole of NOD2IL-1β expressionMaternal-fetal interfaceActivation of NOD2IL-1β productionBacterial muramyl dipeptideAntiphospholipid antibodiesCommon bacterial componentsPregnancy complicationsPregnancy outcomesAdverse outcomesIL-1βTrophoblast responsesExtravillous trophoblastsHigh riskPreeclampsiaDanger signalsBacterial infectionsVEGF secretionInflammationMacrophage Migration Inhibitory Factor Regulates U1 Small Nuclear RNP Immune Complex–Mediated Activation of the NLRP3 Inflammasome
Shin MS, Kang Y, Wahl ER, Park HJ, Lazova R, Leng L, Mamula M, Krishnaswamy S, Bucala R, Kang I. Macrophage Migration Inhibitory Factor Regulates U1 Small Nuclear RNP Immune Complex–Mediated Activation of the NLRP3 Inflammasome. Arthritis & Rheumatology 2018, 71: 109-120. PMID: 30009530, PMCID: PMC6310104, DOI: 10.1002/art.40672.Peer-Reviewed Original ResearchMeSH KeywordsAntigen-Antibody ComplexAutoantibodiesBlotting, WesternCARD Signaling Adaptor ProteinsEnzyme-Linked Immunosorbent AssayFlow CytometryHumansInflammasomesInterleukin-1betaIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMass SpectrometryMonocytesNLR Family, Pyrin Domain-Containing 3 ProteinReceptors, ImmunologicRibonucleoprotein, U1 Small NuclearConceptsMacrophage migration inhibitory factorSystemic lupus erythematosusMigration inhibitory factorNLRP3 inflammasome activationImmune complexesIL-1βNLRP3 inflammasomeHuman monocytesInflammasome activationExpression of MIFProduction of MIFInhibitory factorCaspase-1IL-1β levelsIL-1β productionEnzyme-linked immunosorbentQuantitative polymerase chain reactionHigh expression alleleLupus patientsMIF productionMIF receptorInflammatory characteristicsLupus erythematosusInterleukin-1βPolymerase chain reaction
2017
Viral Infection Sensitizes Human Fetal Membranes to Bacterial Lipopolysaccharide by MERTK Inhibition and Inflammasome Activation.
Cross SN, Potter JA, Aldo P, Kwon JY, Pitruzzello M, Tong M, Guller S, Rothlin CV, Mor G, Abrahams VM. Viral Infection Sensitizes Human Fetal Membranes to Bacterial Lipopolysaccharide by MERTK Inhibition and Inflammasome Activation. The Journal Of Immunology 2017, 199: 2885-2895. PMID: 28916522, PMCID: PMC5659726, DOI: 10.4049/jimmunol.1700870.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsc-Mer Tyrosine KinaseCells, CulturedChorioamnionitisExtraembryonic MembranesFemaleGammaherpesvirinaeHerpesviridae InfectionsHerpesvirus 2, HumanHumansImmunizationInflammasomesIntercellular Signaling Peptides and ProteinsInterleukin-1betaLipopolysaccharidesMiceMice, Inbred C57BLMice, KnockoutPregnancyPremature BirthProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesConceptsFetal membranesViral infectionImmune responseTAM receptorsSubsequent preterm birthAdverse pregnancy outcomesIL-1β productionIL-1β responseHerpes viral infectionsInnate immune responseVivo mouse modelHuman fetal membranesAggravated inflammationIL-1β processingPregnancy outcomesPreterm birthAssociated complicationsPremature rupturePregnant womenLocal infectionInflammasome activationMerTK inhibitionMouse modelBacterial LPSLigand expressionMacrophage Migration Inhibitory Factor Serves As an Upstream Regulator of NLRP3 Expression and Subsequent IL-1beta Production in Human Monocytes in Response to Lupus U1-snRNP Immune Complex
Shin M, Kang Y, Leng L, Bucala R, Kang I. Macrophage Migration Inhibitory Factor Serves As an Upstream Regulator of NLRP3 Expression and Subsequent IL-1beta Production in Human Monocytes in Response to Lupus U1-snRNP Immune Complex. The Journal Of Immunology 2017, 198: 210.3-210.3. DOI: 10.4049/jimmunol.198.supp.210.3.Peer-Reviewed Original ResearchMacrophage migration inhibitory factorMigration inhibitory factorIL-1β productionImmune complexesIL-1βHuman monocytesNLRP3 inflammasomeProduction of MIFExogenous MIFInhibitory factorMIF gene polymorphismsSerum MIF levelsLupus-prone miceSystemic lupus erythematosusExpression of NLRP3Subsequent tissue injuryIL-1beta productionNF-kB activationCaspase-1 activationMIF antagonistMIF levelsLupus patientsLupus erythematosusNLRP3 expressionAutoantibody production
2016
Chitinase 3-Like 1 (Chil1) Regulates Survival and Macrophage-Mediated Interleukin-1β and Tumor Necrosis Factor Alpha during Pseudomonas aeruginosa Pneumonia
Marion CR, Wang J, Sharma L, Losier A, Lui W, Andrews N, Elias JA, Kazmierczak BI, Roy CR, Dela Cruz CS. Chitinase 3-Like 1 (Chil1) Regulates Survival and Macrophage-Mediated Interleukin-1β and Tumor Necrosis Factor Alpha during Pseudomonas aeruginosa Pneumonia. Infection And Immunity 2016, 84: 2094-2104. PMID: 27141083, PMCID: PMC4936356, DOI: 10.1128/iai.00055-16.Peer-Reviewed Original ResearchConceptsBone marrow-derived macrophagesTumor necrosis factor alphaExcessive IL-1β productionNecrosis factor alphaIL-1β productionWT miceAeruginosa pneumoniaFactor alphaChitinase 3Lung parenchymal damageHospital-acquired pneumoniaIL-13 receptor α2Pseudomonas aeruginosa pneumoniaP. aeruginosa pneumoniaDecreased survival timeStreptococcus pneumoniae infectionHost inflammatory responseP. aeruginosa infectionInterleukin-1β productionMarrow-derived macrophagesHost tissue damageP. aeruginosaHost tolerancePneumoniae infectionParenchymal damage
2014
Glucose and Metformin Modulate Human First Trimester Trophoblast Function: a Model and Potential Therapy for Diabetes‐Associated Uteroplacental Insufficiency
Han CS, Herrin MA, Pitruzzello MC, Mulla MJ, Werner EF, Pettker CM, Flannery CA, Abrahams VM. Glucose and Metformin Modulate Human First Trimester Trophoblast Function: a Model and Potential Therapy for Diabetes‐Associated Uteroplacental Insufficiency. American Journal Of Reproductive Immunology 2014, 73: 362-371. PMID: 25394884, PMCID: PMC4356646, DOI: 10.1111/aji.12339.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenesis Inducing AgentsAntigens, CDCarrier ProteinsCell LineCell MovementChemokine CCL5Chemokine CXCL1Diabetes ComplicationsDiabetes MellitusEndoglinFemaleGlucoseGranulocyte Colony-Stimulating FactorHumansInflammationInterleukinsMetforminNLR Family, Pyrin Domain-Containing 3 ProteinPlacentaPre-EclampsiaPregnancyPregnancy Trimester, FirstReceptors, Cell SurfaceTrophoblastsUterusVascular Endothelial Growth Factor Receptor-1ConceptsHuman first trimester trophoblast cell lineAnti-angiogenic factor sFlt-1First trimester trophoblast cell lineNalp3/ASC inflammasomeInflammatory cytokines/chemokinesFirst trimester trophoblast cellsGlucose-induced inflammationRisk of preeclampsiaCytokines/chemokinesAbsence of metforminIL-1β productionIL-1β secretionTrophoblast cell lineUteroplacental insufficiencyIL-1βIL-6SFlt-1Trophoblast functionsIL-8Pathogenic roleInflammatory responseASC inflammasomeSupernatant cytokinesPotential therapyExcess glucoseAdipose Tissue Macrophages Promote Myelopoiesis and Monocytosis in Obesity
Nagareddy PR, Kraakman M, Masters SL, Stirzaker RA, Gorman DJ, Grant RW, Dragoljevic D, Hong ES, Abdel-Latif A, Smyth SS, Choi SH, Korner J, Bornfeldt KE, Fisher EA, Dixit VD, Tall AR, Goldberg IJ, Murphy AJ. Adipose Tissue Macrophages Promote Myelopoiesis and Monocytosis in Obesity. Cell Metabolism 2014, 19: 821-835. PMID: 24807222, PMCID: PMC4048939, DOI: 10.1016/j.cmet.2014.03.029.Peer-Reviewed Original ResearchMeSH KeywordsAdipose TissueAnimalsBone MarrowCarrier ProteinsCell ProliferationHumansInflammasomesInterleukin-1betaMacrophagesMaleMiceMice, Inbred C57BLMonocytesMyeloid Differentiation Factor 88MyelopoiesisNeutrophilsNLR Family, Pyrin Domain-Containing 3 ProteinObesityReceptors, Interleukin-1Toll-Like Receptor 4ConceptsAT macrophagesInsulin resistanceNLRP3 inflammasome-dependent IL-1β productionAdipose tissueMyeloid progenitorsTLR4/MyD88Infiltration of macrophagesBone marrow myeloid progenitorsIL-1β productionS100A8/A9IL-1 receptorMarrow myeloid progenitorsProduction of monocytesAT inflammationLean recipientsNLRP3-ILTLR4 ligandIL-1βMurine modelMyeloid progenitor proliferationProminent monocytosisObesityMonocytosisWeight lossProgenitor proliferation
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 activationPathwaySignalingResponseInterleukinStimuliDiseaseA Role for Uric Acid and the Nalp3 Inflammasome in Antiphospholipid Antibody-Induced IL-1β Production by Human First Trimester Trophoblast
Mulla MJ, Salmon JE, Chamley LW, Brosens JJ, Boeras CM, Kavathas PB, Abrahams VM. A Role for Uric Acid and the Nalp3 Inflammasome in Antiphospholipid Antibody-Induced IL-1β Production by Human First Trimester Trophoblast. PLOS ONE 2013, 8: e65237. PMID: 23762324, PMCID: PMC3675211, DOI: 10.1371/journal.pone.0065237.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, AntiphospholipidAntiphospholipid Syndromebeta 2-Glycoprotein ICARD Signaling Adaptor ProteinsCarrier ProteinsCaspase 1Cell LineCytoskeletal ProteinsFemaleGene Expression RegulationHumansInflammasomesInterleukin-1betaMiceNLR Family, Pyrin Domain-Containing 3 ProteinPregnancyPregnancy Trimester, FirstProtein PrecursorsSignal TransductionToll-Like Receptor 4TrophoblastsUric AcidConceptsIL-1β productionIntrauterine growth restrictionIL-1β secretionAntiphospholipid syndromeIL-1β processingAntiphospholipid antibodiesIL-1βHuman first trimester trophoblast cell lineFirst trimester trophoblast cell lineUric acidNalp3/ASC inflammasomeHuman first trimester trophoblast cellsToll-like receptor 4Human first-trimester trophoblastsFirst trimester trophoblast cellsAnti-β2GPI AbsAdverse pregnancy outcomesAnti-β2GPI antibodiesRecurrent pregnancy lossTLR4-dependent mannerApoptosis-associated speck-like proteinMaternal-fetal interfaceFirst trimester trophoblastsSpeck-like proteinTrophoblast cell lineSelf dsDNA induces IL-1β production from human monocytes by activating NLRP3 inflammasome in the presence of anti-dsDNA antibodies (P4083)
Shin M, Kang Y, Lee N, Kim S, Kang K, Lazova R, Kang I. Self dsDNA induces IL-1β production from human monocytes by activating NLRP3 inflammasome in the presence of anti-dsDNA antibodies (P4083). The Journal Of Immunology 2013, 190: 127.13-127.13. DOI: 10.4049/jimmunol.190.supp.127.13.Peer-Reviewed Original ResearchIL-1β productionAnti-dsDNA antibodiesIL-1βHuman monocytesReactive oxygen speciesCell responsesIL-1β dependent mannerPro-inflammatory cytokines IL-1βPeripheral blood mononuclear cellsSelf-nuclear antigensIL-17 productionSystemic lupus erythematosusInnate immune cellsBlood mononuclear cellsPathogenesis of lupusAntibody-positive seraCytokines IL-1βLupus pathogenesisLupus patientsLupus erythematosusAutoimmune responseCutaneous lesionsMononuclear cellsImmune cellsNLRP3 inflammasomeFlagellar Motility Is a Key Determinant of the Magnitude of the Inflammasome Response to Pseudomonas aeruginosa
Patankar YR, Lovewell RR, Poynter ME, Jyot J, Kazmierczak BI, Berwin B. Flagellar Motility Is a Key Determinant of the Magnitude of the Inflammasome Response to Pseudomonas aeruginosa. Infection And Immunity 2013, 81: 2043-2052. PMID: 23529619, PMCID: PMC3676033, DOI: 10.1128/iai.00054-13.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosis Regulatory ProteinsCARD Signaling Adaptor ProteinsCaspase 1Cell DeathCytoskeletal ProteinsDendritic CellsFlagellaGene Expression RegulationInflammasomesInterleukin-1betaMacrophages, PeritonealMiceMice, Inbred C57BLMice, KnockoutMovementPhagocytosisPseudomonas aeruginosaPseudomonas InfectionsConceptsBacterial motilityFlagellar motilityBacterial flagellar motilityInnate immune systemWild-type P. aeruginosaInflammasome activationP. aeruginosaFlagellar expressionIngest bacteriaBone marrow-derived dendritic cellsImmune systemNLRC4 inflammasome activationBacterial associationsCaspase-1 activationBacterial interactionsMarrow-derived dendritic cellsChronic Pseudomonas aeruginosa infectionIL-1β levelsCell surfacePseudomonas aeruginosa infectionIL-1β productionInflammasome responseMotilityDendritic cellsAeruginosa infectionSelf Double-Stranded (ds)DNA Induces IL-1β Production from Human Monocytes by Activating NLRP3 Inflammasome in the Presence of Anti–dsDNA Antibodies
Shin MS, Kang Y, Lee N, Wahl ER, Kim SH, Kang KS, Lazova R, Kang I. Self Double-Stranded (ds)DNA Induces IL-1β Production from Human Monocytes by Activating NLRP3 Inflammasome in the Presence of Anti–dsDNA Antibodies. The Journal Of Immunology 2013, 190: 1407-1415. PMID: 23315075, PMCID: PMC3563755, DOI: 10.4049/jimmunol.1201195.Peer-Reviewed Original ResearchConceptsIL-1β productionIL-1βHuman monocytesReactive oxygen speciesOligomerization domain-like receptor family pyrinCell responsesProinflammatory cytokines IL-1βTh17 cell responseIL-17 productionAnti-dsDNA antibodiesSystemic lupus erythematosusInnate immune cellsAnti-dsDNA AbsPathogenesis of lupusCytokines IL-1βLupus pathogenesisLupus patientsFamily pyrinLupus erythematosusAutoimmune responseCutaneous lesionsImmune cellsT cellsNuclear AgsPathogenic hallmark
2012
Nod1, but not the ASC inflammasome, contributes to induction of IL-1β secretion in human trophoblasts after sensing of Chlamydia trachomatis
Kavathas PB, Boeras CM, Mulla MJ, Abrahams VM. Nod1, but not the ASC inflammasome, contributes to induction of IL-1β secretion in human trophoblasts after sensing of Chlamydia trachomatis. Mucosal Immunology 2012, 6: 235-243. PMID: 22763410, PMCID: PMC3465624, DOI: 10.1038/mi.2012.63.Peer-Reviewed Original ResearchMeSH KeywordsCARD Signaling Adaptor ProteinsCarrier ProteinsCell LineChlamydia trachomatisCytoskeletal ProteinsGene ExpressionHumansInflammasomesInterleukin-1betaMyeloid Differentiation Factor 88NLR Family, Pyrin Domain-Containing 3 ProteinNod1 Signaling Adaptor ProteinToll-Like Receptor 2Toll-Like Receptor 4TrophoblastsConceptsIL-1β secretionToll-like receptorsCT infectionIL-1βASC inflammasomeChlamydia trachomatisKey Toll-like receptorsNalp3/ASC inflammasomePro-inflammatory cytokinesIL-1β mRNAIL-1β productionInnate immune pathwaysNOD-like receptorsHuman trophoblast cellsIntracellular bacterial pathogenChlamydia infectionImmune pathwaysObligate intracellular bacterial pathogenTrophoblast cellsHuman trophoblastsCaspase-1InfectionSecretionInflammasomeNOD1U1-Small Nuclear Ribonucleoprotein Activates the NLRP3 Inflammasome in Human Monocytes
Shin MS, Kang Y, Lee N, Kim SH, Kang KS, Lazova R, Kang I. U1-Small Nuclear Ribonucleoprotein Activates the NLRP3 Inflammasome in Human Monocytes. The Journal Of Immunology 2012, 188: 4769-4775. PMID: 22490866, PMCID: PMC3347773, DOI: 10.4049/jimmunol.1103355.Peer-Reviewed Original ResearchConceptsU1 snRNPNuclear ribonucleoproteinSystemic lupus erythematosusIL-1β productionU1 small nuclear RNAU1 small nuclear ribonucleoproteinSmall nuclear ribonucleoproteinCytosolic protein complexesLupus erythematosusAutoimmune diseasesProtein complexesMicrobial nucleic acidsNuclear RNAPre-mRNAHuman monocytesNOD-like receptor familyReactive oxygen speciesEndogenous DNAReceptor familyMolecular complexesOxygen speciesRibonucleoproteinTLR7/8 pathwayIL-1βNuclear moleculesU1-snRNP activates the NLRP3 inflammasome in human monocytes (171.7)
Shin M, Kang Y, Lee N, Kang K, Lazova R, Kang I. U1-snRNP activates the NLRP3 inflammasome in human monocytes (171.7). The Journal Of Immunology 2012, 188: 171.7-171.7. DOI: 10.4049/jimmunol.188.supp.171.7.Peer-Reviewed Original ResearchSystemic lupus erythematosusIL-1β productionU1 snRNPAutoimmune diseasesIL-1βCaspase-1Human monocytesReactive oxygen speciesU1 small nuclear RNAU1 small nuclear ribonucleoproteinCytosolic protein complexesLupus erythematosusNLRP3 inflammasomeMicrobial nucleic acidsNLRP3Protein complexesNuclear RNANuclear ribonucleoproteinPre-mRNAEndogenous DNAMonocytesAntibodiesPotential roleCD14Inflammasome
2011
Uric Acid Induces Trophoblast IL‐1β Production Via the Inflammasome: Implications for the Pathogenesis of Preeclampsia
Mulla MJ, Myrtolli K, Potter J, Boeras C, Kavathas PB, Sfakianaki AK, Tadesse S, Norwitz ER, Guller S, Abrahams VM. Uric Acid Induces Trophoblast IL‐1β Production Via the Inflammasome: Implications for the Pathogenesis of Preeclampsia. American Journal Of Reproductive Immunology 2011, 65: 542-548. PMID: 21352397, PMCID: PMC3114103, DOI: 10.1111/j.1600-0897.2010.00960.x.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsCARD Signaling Adaptor ProteinsCarrier ProteinsCaspase 1Cell LineCytoskeletal ProteinsDisease ProgressionEnzyme ActivationFemaleGene Expression Regulation, DevelopmentalHumansHyperuricemiaInflammasomesInterleukin-1betaMaternal-Fetal RelationsNLR Family, Pyrin Domain-Containing 3 ProteinNLR ProteinsPre-EclampsiaPregnancyTrophoblastsUric AcidConceptsIL-1β secretionIL-1β productionMonosodium urateTrophoblast cellsUric acidFirst trimester trophoblast cellsAdverse pregnancy outcomesPathogenesis of preeclampsiaMaternal-fetal interfaceInduction of inflammationActive IL-1βNOD-like receptorsThird trimester trophoblastActive caspase-1Uric acid increasesCaspase-1 activationIL-1β processingPregnancy outcomesInflammatory dysregulationPlacental dysfunctionClinical manifestationsIL-1βInflammasome activationNALP3 inflammasomePreeclampsia
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