2023
Leptin-Mediated Induction of IL-6 Expression in Hofbauer Cells Contributes to Preeclampsia Pathogenesis
Ozmen A, Nwabuobi C, Tang Z, Guo X, Larsen K, Guller S, Blas J, Moore M, Kayisli U, Lockwood C, Guzeloglu-Kayisli O. Leptin-Mediated Induction of IL-6 Expression in Hofbauer Cells Contributes to Preeclampsia Pathogenesis. International Journal Of Molecular Sciences 2023, 25: 135. PMID: 38203306, PMCID: PMC10778808, DOI: 10.3390/ijms25010135.Peer-Reviewed Original ResearchMeSH KeywordsFemaleHumansInterleukin-6LeptinNF-kappa BPlacentaPre-EclampsiaPregnancySTAT5 Transcription FactorConceptsIL-6 expressionHofbauer cellsP65 NF-κBIL-6NF-κBLeptin levelsPreeclampsia pathogenesisElevated serum interleukin-6 levelsSerum interleukin-6 levelsERK1/2 MAPKInterleukin-6 levelsPro-inflammatory phenotypeAnti-inflammatory phenotypeLeptin receptor expressionIL-6 productionPathogenesis of PEPlacental leptin productionPhosphorylation levelsERK1/2 MAPK inhibitorIL-6 regulationConcentration-dependent mannerPE patientsHuman pregnancySecond trimesterLeptin concentrations
2019
Thermal stability of cytokines: A review
Simpson S, Kaislasuo J, Guller S, Pal L. Thermal stability of cytokines: A review. Cytokine 2019, 125: 154829. PMID: 31472404, DOI: 10.1016/j.cyto.2019.154829.Peer-Reviewed Original Research
2016
Inflammatory processes are specifically enhanced in endothelial cells by placental-derived TNF-α: Implications in preeclampsia (PE)
Shaw J, Tang Z, Schneider H, Saljé K, Hansson SR, Guller S. Inflammatory processes are specifically enhanced in endothelial cells by placental-derived TNF-α: Implications in preeclampsia (PE). Placenta 2016, 43: 1-8. PMID: 27324092, DOI: 10.1016/j.placenta.2016.04.015.Peer-Reviewed Original ResearchConceptsPro-inflammatory cytokine secretionMaternal perfusateCytokine secretionEndothelial dysfunctionActivation markersEndothelial cellsTNF-α blocking antibodyDual perfusion modelMaternal endothelial dysfunctionPro-inflammatory cytokinesMCP-1 secretionTNF-α actionEndothelial cell linePlacental pathophysiologyEndothelial activationIL-6IL-8Maternal endotheliumInflammatory processDual perfusionMaternal circulationBlocking antibodiesPreeclampsiaTNFPerfusion model
2014
Toll‐like Receptor‐Mediated Responses by Placental Hofbauer Cells (HBCs): A Potential Pro‐Inflammatory Role for Fetal M2 Macrophages
Young OM, Tang Z, Niven‐Fairchild T, Tadesse S, Krikun G, Norwitz ER, Mor G, Abrahams VM, Guller S. Toll‐like Receptor‐Mediated Responses by Placental Hofbauer Cells (HBCs): A Potential Pro‐Inflammatory Role for Fetal M2 Macrophages. American Journal Of Reproductive Immunology 2014, 73: 22-35. PMID: 25345551, PMCID: PMC4268350, DOI: 10.1111/aji.12336.Peer-Reviewed Original ResearchConceptsHofbauer cellsHuman umbilical vein endothelial cellsM2 macrophagesTLR-3TLR-4Potential pro-inflammatory roleToll-like receptor functionPlacental villous coreAdverse pregnancy outcomesPro-inflammatory rolePlacental Hofbauer cellsIL-6 secretionToll-like receptorsPolycytidylic acid treatmentUmbilical vein endothelial cellsFetal inflammationPregnancy outcomesVein endothelial cellsTLR agonistsTLR-2Cytokine secretionInflammatory responseVillous corePlacental fibroblastsReceptor function
2012
Cutting‐Edge Report: TLR10 Plays a Role in Mediating Bacterial Peptidoglycan‐Induced Trophoblast Apoptosis
Mulla MJ, Myrtolli K, Tadesse S, Stanwood NL, Gariepy A, Guller S, Norwitz ER, Abrahams VM. Cutting‐Edge Report: TLR10 Plays a Role in Mediating Bacterial Peptidoglycan‐Induced Trophoblast Apoptosis. American Journal Of Reproductive Immunology 2012, 69: 449-453. PMID: 23279063, PMCID: PMC3620725, DOI: 10.1111/aji.12065.Peer-Reviewed Original ResearchConceptsIL-6 secretionTrophoblast apoptosisTLR2 coreceptorsHuman trophoblast cell lineIntrauterine bacterial infectionFirst-trimester human trophoblast cell lineThird-trimester human placental tissueHuman placental tissueTrophoblast cell linePositive bacterial componentsTLR10 expressionPreterm laborThird trimesterCaspase-3 activityIL-6TLR2 activationPlacental tissuePlacental apoptosisBacterial infectionsTLR10Bacterial componentsBacterial peptidoglycanTrophoblastCell linesApoptosisLipopolysaccharide 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