2021
Dissection of Barrier Dysfunction in Organoid-Derived Human Intestinal Epithelia Induced by Giardia duodenalis
Holthaus D, Kraft M, Krug S, Wolf S, Müller A, Delgado Betancourt E, Schorr M, Holland G, Knauf F, Schulzke J, Aebischer T, Klotz C. Dissection of Barrier Dysfunction in Organoid-Derived Human Intestinal Epithelia Induced by Giardia duodenalis. Gastroenterology 2021, 162: 844-858. PMID: 34822802, DOI: 10.1053/j.gastro.2021.11.022.Peer-Reviewed Original ResearchMeSH KeywordsApoptosisCaco-2 CellsChloridesCyclic AMPCyclic AMP-Dependent Protein KinasesCystic Fibrosis Transmembrane Conductance RegulatorDuodenumElectric ImpedanceGiardia lambliaGiardiasisHumansInterleukin-1Intestinal MucosaIon TransportNF-kappa BOrganoidsParasite LoadSignal TransductionSolute Carrier Family 12, Member 2Tight JunctionsTranscriptomeTumor Necrosis Factor-alphaConceptsG. duodenalis infectionBarrier dysfunctionGiardia duodenalisHuman duodenal tissueIntestinal barrier dysfunctionHuman intestinal epitheliumResponse element-binding proteinTight junction compositionProtozoan Giardia duodenalisAdequate cellular modelsChronic casesMajor expression changesPathophysiological mechanismsBarrier breakdownDuodenal mucosaGastrointestinal illnessDuodenal tissueBarrier lossPathogenic eventsHuman organoid systemEpithelial barrierTranswell systemChloride secretionIntestinal epitheliumTight junction components
2019
Tumor 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 function