2017
Metabolomics reveals new metabolic perturbations in children with type 1 diabetes
Galderisi A, Pirillo P, Moret V, Stocchero M, Gucciardi A, Perilongo G, Moretti C, Monciotti C, Giordano G, Baraldi E. Metabolomics reveals new metabolic perturbations in children with type 1 diabetes. Pediatric Diabetes 2017, 19: 59-67. PMID: 28401628, DOI: 10.1111/pedi.12524.Peer-Reviewed Original ResearchConceptsBody mass indexType 1 diabetesHealthy controlsPubertal statusExcess of cortisolMetabolome of childrenPediatric diabetes clinicMacrovascular complicationsDiabetes clinicDisease durationNeuronal damagePediatric patientsClinical featuresMass indexCase groupTryptophan catabolitesHealthy peersUrinary metabolitesUrinary samplesBacterial productsT1DUntargeted metabolomics approachMetabolic perturbationsDiabetesPatientsInflammation: A Double-Edged Sword in the Response to Pseudomonas aeruginosa Infection
Lin CK, Kazmierczak BI. Inflammation: A Double-Edged Sword in the Response to Pseudomonas aeruginosa Infection. Journal Of Innate Immunity 2017, 9: 250-261. PMID: 28222444, PMCID: PMC5469373, DOI: 10.1159/000455857.Peer-Reviewed Original ResearchConceptsP. aeruginosa pulmonary infectionInnate immune recognitionPseudomonas aeruginosa infectionInflamed airwaysPulmonary infectionAcute infectionAdjunct therapyChronic infectionBarrier defenseAeruginosa infectionAnatomic sitesPathogen clearanceBacterial productsImmune recognitionInnate immunityInfectionHost outcomesResistant pathogensP. aeruginosa adaptationInflammationP. aeruginosaPathogen persistenceDouble-edged swordPseudomonas aeruginosaDefense mechanisms
2016
Increased susceptibility of Cftr−/− mice to LPS-induced lung remodeling
Bruscia E, Zhang P, Barone C, Scholte BJ, Homer R, Krause D, Egan ME. Increased susceptibility of Cftr−/− mice to LPS-induced lung remodeling. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2016, 310: l711-l719. PMID: 26851259, PMCID: PMC4836110, DOI: 10.1152/ajplung.00284.2015.Peer-Reviewed Original ResearchConceptsLung pathologyCF miceImmune responseWT miceChronic inflammationCystic fibrosisAbnormal immune responseChronic pulmonary infectionPersistent immune responseWild-type littermatesCF mouse modelsPseudomonas aeruginosa lipopolysaccharideCF lung pathologyPulmonary infectionChronic administrationLPS exposurePersistent inflammationLung remodelingWT littermatesLung tissueOverall pathologyMouse modelInflammationChronic exposureBacterial products
2011
Corrections: Viral Infection of the Placenta Leads to Fetal Inflammation and Sensitization to Bacterial Products Predisposing to Preterm Labor
Cardenas I, Means R, Aldo P, Koga K, Lang S, Booth C, Manzur A, Oyarzun E, Romero R, Mor G. Corrections: Viral Infection of the Placenta Leads to Fetal Inflammation and Sensitization to Bacterial Products Predisposing to Preterm Labor. The Journal Of Immunology 2011, 187: 2835-2835. DOI: 10.4049/jimmunol.1190048.Peer-Reviewed Original Research
2010
Focal Increases of Fetal Macrophages in Placentas from Pregnancies with Histological Chorioamnionitis: Potential Role of Fibroblast Monocyte Chemotactic Protein‐1
Toti P, Arcuri F, Tang Z, Schatz F, Zambrano E, Mor G, Niven‐Fairchild T, Abrahams VM, Krikun G, Lockwood CJ, Guller S. Focal Increases of Fetal Macrophages in Placentas from Pregnancies with Histological Chorioamnionitis: Potential Role of Fibroblast Monocyte Chemotactic Protein‐1. American Journal Of Reproductive Immunology 2010, 65: 470-479. PMID: 21087336, PMCID: PMC3071455, DOI: 10.1111/j.1600-0897.2010.00927.x.Peer-Reviewed Original ResearchConceptsHistopathological chorioamnionitisMCP-1 mRNAFocal increaseMonocyte chemotactic protein-1Subset of pregnanciesAdverse neonatal outcomesProtein expressionPro-inflammatory cytokinesMaternal-fetal interfaceChemotactic protein-1MCP-1 expressionTerm placental villiHistological chorioamnionitisNeonatal outcomesCytokine cascadeIL-1βInflammatory cytokinesQuantitative real-time PCRFetal monocytesReal-time PCRHuman term placental villiPlacental villiControl groupBacterial productsTreatment of fibroblastsPlacental Viral Infection Sensitizes to Endotoxin‐Induced Pre‐Term Labor: A Double Hit Hypothesis
Cardenas I, Mor G, Aldo P, Lang SM, Stabach P, Sharp A, Romero R, Mazaki‐Tovi S, Gervasi M, Means RE. Placental Viral Infection Sensitizes to Endotoxin‐Induced Pre‐Term Labor: A Double Hit Hypothesis. American Journal Of Reproductive Immunology 2010, 65: 110-117. PMID: 20712808, PMCID: PMC3025809, DOI: 10.1111/j.1600-0897.2010.00908.x.Peer-Reviewed Original ResearchConceptsPre-term labourPre-term deliveryDouble-hit hypothesisViral infectionPregnancy outcomesBacterial infectionsCytokine/chemokine profilesHit hypothesisConcurrent bacterial infectionFetal immune responsePro-inflammatory cytokinesWild-type miceHuman primary trophoblastsMurine gammaherpesvirus 68Fetal deathChemokine profilesPoor prognosisPregnant womenAdverse outcomesPregnant miceLPS treatmentImmune responseBacterial productsPrimary trophoblastsLow dosesViral Infection of the Placenta Leads to Fetal Inflammation and Sensitization to Bacterial Products Predisposing to Preterm Labor
Cardenas I, Means RE, Aldo P, Koga K, Lang SM, Booth C, Manzur A, Oyarzun E, Romero R, Mor G. Viral Infection of the Placenta Leads to Fetal Inflammation and Sensitization to Bacterial Products Predisposing to Preterm Labor. The Journal Of Immunology 2010, 185: 1248-1257. PMID: 20554966, PMCID: PMC3041595, DOI: 10.4049/jimmunol.1000289.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBacterial InfectionsCell LineCells, CulturedCytokinesFemaleFetal DiseasesFetusHost-Pathogen InteractionsHumansImmunohistochemistryInflammationMaternal-Fetal ExchangeMiceMice, Inbred C57BLMice, KnockoutNIH 3T3 CellsObstetric Labor, PrematurePlacentaPlacenta DiseasesPregnancyPregnancy Complications, InfectiousRhadinovirusToll-Like Receptor 3Virus DiseasesConceptsViral infectionPreterm laborBacterial productsFetal inflammatory responseMaternal immune systemFetal transmissionFetal inflammationNonpregnant populationOrgan damagePregnant womenPregnant mothersPlacental unitInflammatory responseImmunological roleAnimal modelsImmune systemInfectionPlacentaMicrobial infectionsFetusesDevelopmental deficienciesMothersDetrimental effectsPandemicInflammation
2009
Salmonella Typhimurium Type III Secretion Effectors Stimulate Innate Immune Responses in Cultured Epithelial Cells
Bruno VM, Hannemann S, Lara-Tejero M, Flavell RA, Kleinstein SH, Galán JE. Salmonella Typhimurium Type III Secretion Effectors Stimulate Innate Immune Responses in Cultured Epithelial Cells. PLOS Pathogens 2009, 5: e1000538. PMID: 19662166, PMCID: PMC2714975, DOI: 10.1371/journal.ppat.1000538.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBacterial ProteinsBlotting, WesternCell LineColitisEpithelial CellsGene ExpressionGene Expression ProfilingGuanine Nucleotide Exchange FactorsHumansImmunity, InnateMiceMitogen-Activated Protein Kinase KinasesMyotonin-Protein KinaseNF-kappa BOligonucleotide Array Sequence AnalysisProtein Serine-Threonine KinasesReverse Transcriptase Polymerase Chain ReactionSalmonella InfectionsSalmonella typhimuriumSignal TransductionTranscription, GeneticConceptsInnate immune receptorsInnate immune responseIntestinal inflammationImmune responseEpithelial cellsBacterial productsIntestinal inflammatory pathologyImmune receptorsCultured epithelial cellsEnteric pathogen Salmonella typhimuriumInnate immune systemIntestinal epithelial cellsInflammatory pathologyInflammatory responseType III secretion effectorsImmune systemSalmonella typhimuriumNF-kappaBMitogen-activated protein kinaseEnteric pathogensPathogen Salmonella typhimuriumPathologyReceptorsInflammationType III secretion system
2007
Tumor Necrosis Factor
Pober J. Tumor Necrosis Factor. 2007, 261-265. DOI: 10.1017/cbo9780511546198.032.Peer-Reviewed Original ResearchHemorrhagic necrosisNecrosis factorMediator of cachexiaMediators of inflammationTumor necrosis factorPrimary cellular sourceAdaptive immune systemTNF-like moleculeTime of cloningMajor histocompatibility complexPeyer's patchesEndogenous mediatorsT lymphocytesMast cellsParasitic infectionsTNFBacterial productsExperimental tumorsImmune systemMononuclear phagocytesCellular sourceSmall intestineHistocompatibility complexTNF geneRelated receptors
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply