2023
Epithelial TNF controls cell differentiation and CFTR activity to maintain intestinal mucin homeostasis
Reyes E, Castillo-Azofeifa D, Rispal J, Wald T, Zwick R, Palikuqi B, Mujukian A, Rabizadeh S, Gupta A, Gardner J, Boffelli D, Gartner Z, Klein O. Epithelial TNF controls cell differentiation and CFTR activity to maintain intestinal mucin homeostasis. Journal Of Clinical Investigation 2023, 133: e163591. PMID: 37643009, PMCID: PMC10575728, DOI: 10.1172/jci163591.Peer-Reviewed Original ResearchConceptsCystic fibrosis transmembrane conductance regulatorTumor necrosis factorInflammatory bowel diseaseCell differentiationRegulate mucin productionCystic fibrosis transmembrane conductance regulator inhibitionCystic fibrosis transmembrane conductance regulator activityTumor necrosis factor treatmentInflammatory cytokine tumor necrosis factorAnti-TNF therapyAbsence of tumor necrosis factorTransmembrane conductance regulatorCytokine tumor necrosis factorMucus-producing goblet cellsGenetic mouse modelsUpstream regulatorIncreased mucus accumulationAdult intestineConductance regulatorEpithelial signalsSignaling AxisProgenitor cellsMouse modelNecrosis factorGut transit timeComparative Safety of Biologic Agents in Patients With Inflammatory Bowel Disease With Active or Recent Malignancy: A Multi-Center Cohort Study
Holmer A, Luo J, Russ K, Park S, Yang J, Ertem F, Dueker J, Nguyen V, Hong S, Zenger C, Axelrad J, Sofia A, Petrov J, Al-Bawardy B, Fudman D, Llano E, Dailey J, Jangi S, Khakoo N, Damas O, Barnes E, Scott F, Ungaro R, Singh S, Helping-IBD R. Comparative Safety of Biologic Agents in Patients With Inflammatory Bowel Disease With Active or Recent Malignancy: A Multi-Center Cohort Study. Clinical Gastroenterology And Hepatology 2023, 21: 1598-1606.e5. PMID: 36642291, DOI: 10.1016/j.cgh.2023.01.002.Peer-Reviewed Original ResearchConceptsNon-TNF biologicsInflammatory bowel diseaseProgression-free survivalRecurrence-free survivalTNFα antagonistsActive cancerPrior cancerCohort studyBiologic agentsBowel diseaseRecent cancerMulticenter retrospective cohort studyMulti-center cohort studyIBD disease severityRetrospective cohort studyChoice of biologicsTumor necrosis factorCohort BPrimary outcomeComparable safetyΑ antagonistsComparative safetyCancer recurrenceNecrosis factorPatients
2022
Real-World Evidence Comparing Vedolizumab and Ustekinumab in Antitumor Necrosis Factor-Experienced Patients With Crohn's Disease
Kappelman M, Adimadhyam S, Hou L, Wolfe A, Smith S, Simon A, Moyneur É, Reynolds J, Toh S, Dobes A, Parlett L, Haynes K, Selvan M, Ma Q, Nair V, Burris J, Dorand J, Dawwas G, Lewis J, Long M. Real-World Evidence Comparing Vedolizumab and Ustekinumab in Antitumor Necrosis Factor-Experienced Patients With Crohn's Disease. The American Journal Of Gastroenterology 2022, 118: 674-684. PMID: 36508681, DOI: 10.14309/ajg.0000000000002068.Peer-Reviewed Original ResearchConceptsCrohn's diseaseCause hospitalizationCD hospitalizationsTreatment persistenceSecondary outcomesAntitumor necrosis factor therapyReal-world comparative effectiveness studiesAntitumor necrosis factorLarge US insurerNecrosis factor therapyTreatment persistence ratesAnti-TNF treatmentBaseline clinical characteristicsRetrospective cohort studyComparative effectiveness studiesRoute of administrationDiverse US populationLongitudinal claims dataRefractory populationClinical characteristicsCohort studyFactor therapyPrimary outcomePatient preferencesNecrosis factorRNA Sequencing Reveals Beneficial Effects of Atorvastatin on Endothelial Cells in Acute Kawasaki Disease
Shimizu C, Kim J, He M, Tremoulet A, Hoffman H, Shyy J, Burns J. RNA Sequencing Reveals Beneficial Effects of Atorvastatin on Endothelial Cells in Acute Kawasaki Disease. Journal Of The American Heart Association 2022, 11: e025408. PMID: 35861833, PMCID: PMC9707837, DOI: 10.1161/jaha.122.025408.Peer-Reviewed Original ResearchConceptsKawasaki diseaseGenome-wide transcriptional changesIntravenous immunoglobulinAcute Kawasaki diseaseHuman umbilical vein ECsInflammatory cell infiltrationEndothelial cell dysfunctionTumor necrosis factorTranscriptional changesRNA sequencingKD treatmentAcute phaseMyointimal proliferationCoronary arteryCell infiltrationCultured ECsNecrosis factorCell dysfunctionKD seraInterleukin-1Recruitment pathwayResponse of ECBackground damageSerumPatientsThe Association of Serum Inflammatory Markers and Self-Reported Cognitive Outcomes in Women With Breast Cancer Undergoing Chemotherapy
Zhang Z, Schnell P, Ormiston K, Weinhold K, Kopec R, Lustberg M, Orchard T. The Association of Serum Inflammatory Markers and Self-Reported Cognitive Outcomes in Women With Breast Cancer Undergoing Chemotherapy. Current Developments In Nutrition 2022, 6: 6009258. PMCID: PMC9193788, DOI: 10.1093/cdn/nzac052.025.Peer-Reviewed Original ResearchSerum inflammatory markersInflammatory markersSelf-reported cognitive functionBreast cancerIL-1βTNF-RIICognitive functionIL-8Lower serum IL-1βHigher tumor necrosis factorHigher interleukin-8Lower interleukin-1βSerum omega-3Serum IL-1βLower IL-1βTumor necrosis factorEnzyme-linked immunoassayAdjuvant chemotherapyInterleukin-1βInterleukin-6Cognitive dysfunctionInterleukin-8Necrosis factorQuestionnaire scoresChemotherapyOutcomes of COVID-19 in Patients with Inflammatory Bowel Disease: Comparison with Household Members and the Role of IBD Medications
Sima A, Saberzadeh-Ardestani B, Vahedi H, Fakheri H, Mansour-Ghanaei F, Maleki I, Nasseri-Moghaddam S, Vosoghinia H, Ghadir M, Hormati A, Kasaeian A, Radmard A, Khosravi B, Malekzadeh M, Alatab S, Sadeghi A, Aminisani N, Poustchi H, Gonoudi E, Anushiravani A, Rayatpisheh M, Colombel J, Ungaro R, Malekzadeh R. Outcomes of COVID-19 in Patients with Inflammatory Bowel Disease: Comparison with Household Members and the Role of IBD Medications. Archives Of Iranian Medicine 2022, 25: 17-25. PMID: 35128908, DOI: 10.34172/aim.2022.04.Peer-Reviewed Original ResearchConceptsInflammatory bowel disease patientsInflammatory bowel diseaseGastrointestinal symptomsAnti-tumor necrosis factorAssociated with increased hospitalization ratesBowel diseasePresence of inflammatory bowel diseaseAssociated with higher hospitalization ratesCOVID-19 outcomesAssociated with more severe outcomesAnti-TNF therapyInflammatory bowel disease medicationsHospitalization ratesNon-IBD patientsOutcomes of COVID-19Prospective cohort studyMultivariate logistic regressionEffect of inflammatory bowel diseaseCOVID-19 patientsAssociated with hospitalizationNo significant differenceHigher hospitalization ratesClinical characteristicsCohort studyNecrosis factor
2021
Development and external validation of a diagnostic model for biopsy-proven acute interstitial nephritis using electronic health record data
Moledina DG, Eadon MT, Calderon F, Yamamoto Y, Shaw M, Perazella MA, Simonov M, Luciano R, Schwantes-An TH, Moeckel G, Kashgarian M, Kuperman M, Obeid W, Cantley LG, Parikh CR, Wilson FP. Development and external validation of a diagnostic model for biopsy-proven acute interstitial nephritis using electronic health record data. Nephrology Dialysis Transplantation 2021, 37: 2214-2222. PMID: 34865148, PMCID: PMC9755995, DOI: 10.1093/ndt/gfab346.Peer-Reviewed Original ResearchConceptsAcute interstitial nephritisInterstitial nephritisUrine biomarkersBiopsy-proven acute interstitial nephritisElectronic health record dataExternal validation cohortTypical clinical featuresBlood urea nitrogenTumor necrosis factorCharacteristic curve analysisHealth record dataExternal validationElectronic health recordsAIN diagnosisModest AUCsSerum creatinineCreatinine ratioKidney biopsyClinical featuresValidation cohortNecrosis factorUnrecognized casesInterleukin-9PatientsUrea nitrogenHuman autoinflammatory disease reveals ELF4 as a transcriptional regulator of inflammation
Tyler PM, Bucklin ML, Zhao M, Maher TJ, Rice AJ, Ji W, Warner N, Pan J, Morotti R, McCarthy P, Griffiths A, van Rossum AMC, Hollink IHIM, Dalm VASH, Catanzaro J, Lakhani SA, Muise AM, Lucas CL. Human autoinflammatory disease reveals ELF4 as a transcriptional regulator of inflammation. Nature Immunology 2021, 22: 1118-1126. PMID: 34326534, PMCID: PMC8985851, DOI: 10.1038/s41590-021-00984-4.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCalgranulin ADNA-Binding ProteinsFemaleGene Expression RegulationHereditary Autoinflammatory DiseasesHumansInflammatory Bowel DiseasesInterleukin 1 Receptor Antagonist ProteinLipocalin-2LipopolysaccharidesMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutTh17 CellsTranscription FactorsTranscription, GeneticTriggering Receptor Expressed on Myeloid Cells-1ConceptsInterleukin-1Inflammatory bowel disease (IBD) characteristicsInflammatory immune cellsHuman inflammatory disordersAnti-inflammatory genesTumor necrosis factorHuman autoinflammatory diseasesInnate stimuliHyperinflammatory responseMale patientsNeutrophil chemoattractantDisease characteristicsInflammatory disordersMucosal diseaseImmune cellsInflammation amplifierNecrosis factorUnrelated male patientsAutoinflammatory diseasesMouse modelBroad translational relevanceTranslational relevanceInflammationFunction variantsMouse macrophagesChanges in Serum Fatty Acids and Inflammatory Markers in Postmenopausal Women With Breast Cancer Following Chemotherapy Treatment
Zhang Z, Ormiston K, Schnell P, Kopec R, Lustberg M, Orchard T. Changes in Serum Fatty Acids and Inflammatory Markers in Postmenopausal Women With Breast Cancer Following Chemotherapy Treatment. Current Developments In Nutrition 2021, 5: 5140290. PMCID: PMC8182042, DOI: 10.1093/cdn/nzab036_032.Peer-Reviewed Original ResearchSerum fatty acidsInflammatory markersInterleukin-6Breast cancerSerum cytokinesPostmenopausal breast cancer patientsSerum inflammatory markersBreast cancer survivorsBreast cancer patientsFatty acidsMethods Serum samplesTumor necrosis factorTotal monounsaturated FAsTotal monounsaturated fatty acidsEnzyme-linked immunoassaySerum FCytokine changesPostmenopausal womenInflammatory profileCancer survivorsInflammatory stateCancer patientsIL-8Chemotherapy treatmentNecrosis factorNovel and Emerging Therapies for Inflammatory Bowel Disease
Al-Bawardy B, Shivashankar R, Proctor DD. Novel and Emerging Therapies for Inflammatory Bowel Disease. Frontiers In Pharmacology 2021, 12: 651415. PMID: 33935763, PMCID: PMC8080036, DOI: 10.3389/fphar.2021.651415.BooksInflammatory bowel diseaseBowel diseaseAnti-tumor necrosis factorPotential systemic manifestationsSecondary treatment failureTreatment response ratesJanus kinase inhibitorSelective Janus kinase inhibitorNew therapeutic targetsEmerging TherapiesCurrent biologicsIntestinal inflammationSystemic manifestationsUlcerative colitisCrohn's diseaseTreatment failureSafety profileNecrosis factorTherapeutic targetResponse rateDiseaseKinase inhibitorsTarget agentsInhibitorsTolerability
2020
UFMylation inhibits the proinflammatory capacity of interferon-γ–activated macrophages
Balce DR, Wang YT, McAllaster MR, Dunlap BF, Orvedahl A, Hykes BL, Droit L, Handley SA, Wilen CB, Doench JG, Orchard RC, Stallings CL, Virgin HW. UFMylation inhibits the proinflammatory capacity of interferon-γ–activated macrophages. Proceedings Of The National Academy Of Sciences Of The United States Of America 2020, 118: e2011763118. PMID: 33372156, PMCID: PMC7817147, DOI: 10.1073/pnas.2011763118.Peer-Reviewed Original ResearchConceptsGenome-wide CRISPR knockout screenCRISPR knockout screensEndoplasmic reticulum stress responseRegulation of responsesReticulum stress responseKnockout screensTranscriptional responseGenetic roadmapIFN-γ responsesTumor necrosis factorNegative regulatorMolecular linkUfmylation pathwayUnexpected roleStress responseMacrophage cell lineIFN-γ activationIntracellular pathogensProinflammatory capacityConjugation systemInfluenza infectionCellular immunityIFN-γ effectsNecrosis factorImmune responseMonitoring Atsttrin-Mediated Inhibition of TNFα/NF-κβ Activation Through In Vivo Bioluminescence Imaging
Hettinghouse A, Fu W, Liu C. Monitoring Atsttrin-Mediated Inhibition of TNFα/NF-κβ Activation Through In Vivo Bioluminescence Imaging. Methods In Molecular Biology 2020, 2248: 201-210. PMID: 33185877, PMCID: PMC8140391, DOI: 10.1007/978-1-0716-1130-2_14.Peer-Reviewed Original ResearchConceptsTumor necrosis factorDouble mutant miceNF-κBOverexpression of TNFMutant miceBioluminescence imagingTransgenic reporter mouse modelNF-κB luciferaseNF-κβ activationVivo bioluminescence imagingReporter mouse modelAutoimmune conditionsTNF-TgNF-κβNecrosis factorImmune responseMouse modelMolecular mediatorsTransgenic modelTherapeutic objectivesVivo efficacyProgranulinPotential therapeuticsAtsttrinLuciferase activityUrine interleukin-9 and tumor necrosis factor-α for prognosis of human acute interstitial nephritis
Moledina DG, Wilson FP, Kukova L, Obeid W, Luciano R, Kuperman M, Moeckel GW, Kashgarian M, Perazella MA, Cantley LG, Parikh CR. Urine interleukin-9 and tumor necrosis factor-α for prognosis of human acute interstitial nephritis. Nephrology Dialysis Transplantation 2020, 36: 1851-1858. PMID: 33125471, PMCID: PMC8476079, DOI: 10.1093/ndt/gfaa169.Peer-Reviewed Original ResearchConceptsAcute interstitial nephritisTumor necrosis factorCorticosteroid useIL-9Interstitial nephritisNecrosis factorAcute kidney injuryIL-9 levelsGlomerular filtration rateSubset of patientsCohort of participantsImmunosuppressive therapyTubulointerstitial infiltratesKidney injuryMedian eGFRKidney functionUrine biomarkersInterstitial fibrosisFiltration rateHistological featuresClinical trialsInterleukin-9PatientsEGFRComplete data
2019
Metabolomic Analysis of the Effects of Leptin Replacement Therapy in Patients with Lipodystrophy
Grewal S, Gubbi S, Fosam A, Sedmak C, Sikder S, Talluru H, Brown R, Muniyappa R. Metabolomic Analysis of the Effects of Leptin Replacement Therapy in Patients with Lipodystrophy. Journal Of The Endocrine Society 2019, 4: bvz022. PMID: 32010873, PMCID: PMC6984783, DOI: 10.1210/jendso/bvz022.Peer-Reviewed Original ResearchLeptin replacement therapyOral glucose tolerance testGlucose tolerance testReplacement therapyLeptin therapyTolerance testLeptin-deficient patientsDramatic clinical effectsMetabolomic profilingTumor necrosis factorForms of lipodystrophyHydroxysteroid dehydrogenase 1Body composition measurementsBranched-chain amino acidsBranched-chain amino acid metabolismFatty acid oxidationMetabolomic analysisMechanism of actionMetreleptin therapyClinical effectsFatty acidsLeptin treatmentNecrosis factorTreatment periodFree fatty acidsHepatic insulin sensitivity is improved in high‐fat diet‐fed Park2 knockout mice in association with increased hepatic AMPK activation and reduced steatosis
Edmunds LR, Huckestein BR, Kahn M, Zhang D, Chu Y, Zhang Y, Wendell SG, Shulman GI, Jurczak MJ. Hepatic insulin sensitivity is improved in high‐fat diet‐fed Park2 knockout mice in association with increased hepatic AMPK activation and reduced steatosis. Physiological Reports 2019, 7: e14281. PMID: 31724300, PMCID: PMC6854109, DOI: 10.14814/phy2.14281.Peer-Reviewed Original ResearchConceptsPark2 KO miceHepatic insulin sensitivityKO miceInsulin sensitivityInsulin resistanceShort-term HFD feedingDiet-induced hepatic insulin resistanceWhole-body insulin sensitivityPark2 knockout miceImproved hepatic insulin sensitivityDiet-induced obesityHigh-fat dietBioactive lipid speciesTumor necrosis factorHepatic insulin resistanceHepatic AMPK activationNegative energy balanceEndoplasmic reticulum stress responseRegular chowCytokine levelsHFD feedingReduced steatosisChronic HFDInterleukin-6Necrosis factorProtective effects of GPR120 agonist-programmed macrophages on renal interstitial fibrosis in unilateral ureteral obstruction (UUO) rats
Wang L, Ren X, Tian XF, Cheng XL, Zhao YY, Li QY, Duan ZY, Tian LF, Chen Z, Lu JM, Liang XY, Zhao YF, Fu RG. Protective effects of GPR120 agonist-programmed macrophages on renal interstitial fibrosis in unilateral ureteral obstruction (UUO) rats. Biomedicine & Pharmacotherapy 2019, 117: 109172. PMID: 31261028, DOI: 10.1016/j.biopha.2019.109172.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsbeta CateninBiphenyl CompoundsCytokinesFibrosisGene Expression RegulationKidney DiseasesMacrophages, PeritonealMaleModels, BiologicalPhenotypePhenylpropionatesProtective AgentsRats, Sprague-DawleyReceptors, G-Protein-CoupledSignal TransductionTransforming Growth Factor beta1Ureteral ObstructionVimentinConceptsRenal interstitial fibrosisUnilateral ureteral obstructionInterstitial fibrosisUreteral obstructionProtective effectFree fatty acid receptor GPR120Fatty acid receptor GPR120Unilateral ureteral obstruction operationPeritoneal macrophagesAbnormal expressionExpression of CD206M2 phenotype macrophagesTumor necrosis factorEpithelial-mesenchymal transitionAutologous administrationReceptor GPR120UUO ratsInterleukin-6Intrarenal injectionArginase-1Necrosis factorGPR120 agonistM2 phenotypeΑ-SMATGF-β1Tumor necrosis factor stimulates fibroblast growth factor 23 levels in chronic kidney disease and non-renal inflammation
Egli-Spichtig D, Imenez Silva P, Glaudemans B, Gehring N, Bettoni C, Zhang M, Pastor-Arroyo E, Schönenberger D, Rajski M, Hoogewijs D, Knauf F, Misselwitz B, Frey-Wagner I, Rogler G, Ackermann D, Ponte B, Pruijm M, Leichtle A, Fiedler G, Bochud M, Ballotta V, Hofmann S, Perwad F, Föller M, Lang F, Wenger R, Frew I, Wagner C. Tumor necrosis factor stimulates fibroblast growth factor 23 levels in chronic kidney disease and non-renal inflammation. Kidney International 2019, 96: 890-905. PMID: 31301888, DOI: 10.1016/j.kint.2019.04.009.Peer-Reviewed Original ResearchMeSH KeywordsAdultAnimalsCell LineCohort StudiesDisease Models, AnimalFemaleFibroblast Growth Factor-23Fibroblast Growth FactorsHumansInflammatory Bowel DiseasesInterleukin-10KidneyMaleMiceMice, TransgenicMiddle AgedNuclear Receptor Subfamily 4, Group A, Member 2Primary Cell CultureRenal Insufficiency, ChronicTumor Necrosis Factor-alphaConceptsChronic kidney diseaseTumor necrosis factorPlasma FGF23Kidney diseaseFGF23 expressionFGF23 levelsNecrosis factorGrowth factor 23 levelsFibroblast growth factor 23Inflammatory cytokines tumor necrosis factorCytokines tumor necrosis factorInflammatory bowel diseaseGrowth factor 23Normal kidney functionIL10-deficient micePopulation-based cohortAntibody-mediated neutralizationOrphan nuclear receptor Nurr1Nuclear receptor Nurr1Cause mortalityRenal inflammationTNF neutralizationBowel diseaseFactor 23Kidney functionB cell activation factor (BAFF) induces inflammation in the human fallopian tube leading to tubal pregnancy
Xu J, Luo X, Qu S, Yang G, Shen N. B cell activation factor (BAFF) induces inflammation in the human fallopian tube leading to tubal pregnancy. BMC Pregnancy And Childbirth 2019, 19: 169. PMID: 31088412, PMCID: PMC6518762, DOI: 10.1186/s12884-019-2324-5.Peer-Reviewed Original ResearchConceptsHuman fallopian tubeB cell activation factorTubal pregnancyFallopian tubeSerum levelsBAFF mRNAControl groupBAFF geneTissue samplesBenign uterine diseasesNormal fallopian tubesAdaptive immune responsesTumor necrosis factorTubal epithelial cellsFallopian tube occlusionWestern blotting methodBAFF proteinWhole blood samplesProinflammatory cytokinesIL-6Pregnancy typeActivation factorNecrosis factorPregnancy processUterine disease
2018
Inflammation-Induced Citrullinated Glucose-Regulated Protein 78 Elicits Immune Responses in Human Type 1 Diabetes
Buitinga M, Callebaut A, Sodré F, Crèvecoeur I, Blahnik-Fagan G, Yang ML, Bugliani M, Arribas-Layton D, Marré M, Cook DP, Waelkens E, Mallone R, Piganelli JD, Marchetti P, Mamula MJ, Derua R, James EA, Mathieu C, Overbergh L. Inflammation-Induced Citrullinated Glucose-Regulated Protein 78 Elicits Immune Responses in Human Type 1 Diabetes. Diabetes 2018, 67: 2337-2348. PMID: 30348823, PMCID: PMC6973547, DOI: 10.2337/db18-0295.Peer-Reviewed Original ResearchConceptsType 1 diabetesHuman type 1 diabetesΒ-cellsEffector memory cellsCentral memory cellsT cell responsesHealthy control subjectsTumor necrosis factorUse of HLAElicit immune responsesHuman type 1Glucose-regulated protein 78Generation of neoantigensGeneration of neoepitopesΒ-cell proteinsAutoantibody titersImmune toleranceNovel autoantigenControl subjectsInterleukin-1βInflammatory stressNecrosis factorImmune responseDiabetesELISA techniqueTumor necrosis factor alfa and interleukin 1 alfa induced phosphorylation and degradation of inhibitory kappa B alpha are regulated by estradiol in endometrial cells
Arlıer S, Kayışlı Ü, Arıcı A. Tumor necrosis factor alfa and interleukin 1 alfa induced phosphorylation and degradation of inhibitory kappa B alpha are regulated by estradiol in endometrial cells. Journal Of Turkish Society Of Obstetric And Gynecology 2018, 15: 50-59. PMID: 29662717, PMCID: PMC5894537, DOI: 10.4274/tjod.47700.Peer-Reviewed Original ResearchEndometrial cellsNormal endometriumEctopic endometriumInhibitory kappa B-alphaTranscription factor nuclear factor kappa BInhibitory kappa B (IκBα) proteinMonocyte chemoattractant protein-1Ectopic endometrial cellsHomologous eutopic endometriumNuclear factor kappa BCultured endometrial cellsEffects of estradiolNecrosis factor alfaChemoattractant protein-1Human endometrial cellsRegulation of chemokinesTumor necrosis factorFactor kappa BKappa B alphaUterine endometrial cellsEutopic endometriumInflammatory responseNecrosis factorEndometriumKappa B
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