Probiotics Modulate Intestinal Expression of Nuclear Receptor and Provide Counter-Regulatory Signals to Inflammation-Driven Adipose Tissue Activation 英文参考文献.docVIP
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Probiotics Modulate Intestinal Expression of Nuclear Receptor and Provide Counter-Regulatory Signals to Inflammation-Driven Adipose Tissue Activation 英文参考文献
ProbioticsModulateIntestinalExpressionofNuclear
ReceptorandProvideCounter-RegulatorySignalsto
Inflammation-DrivenAdiposeTissueActivation
AndreaMencarelli1,EleonoraDistrutti2,BarbaraRenga1,ClaudioD’Amore1,SabrinaCipriani1 ,Giuseppe
Palladino1,AnnibaleDonini3,PatriziaRicci3,StefanoFiorucci1*
1DipartimentodiMedicinaClinicaeSperimentale,UniversityofPerugia,Facolta` diMedicinaeChirurgia,ViaGerardoDottorinu1S.AndreadelleFratte,Perugia,Italy,
2AziendaOspedalieradiPerugia,OspedaleSantaMariadellaMisericordia,S.AndreadelleFratte,Perugia,Italy,3DipartimentodiScienzeChirurgiche,Radiologichee
Odontostomatologiche,NuovaFacolta` diMedicinaeChirurgiaSant’AndreadelleFratte,Perugia,Italy
Abstract
Background: Adipocytes from mesenteric white adipose tissue amplify the inflammatory response and participate in
inflammation-driven immune dysfunction in Crohn’s disease by releasing proinflammatory mediators. Peroxisome
proliferator-activatedreceptors(PPAR)-aand-c,pregnanexreceptor(PXR),farnesoidxreceptor(FXR)andliverx-receptor
(LXR) are ligand-activated nuclear receptor that provide counter-regulatory signals to dysregulated immunity and
modulatesadiposetissue.
Aims:Toinvestigatetheexpressionandfunctionofnuclearreceptorsinintestinalandadiposetissuesinarodentmodelof
colitisandmesentericfatfromCrohn’spatientsandtoinvestigatetheirmodulationbyprobiotics.
Methods: Colitis was induced by TNBS administration. Mice were administered vehicle or VSL#3, daily for 10 days.
Abdominal fat explants obtained at surgery from five Crohn’s disease patients and five patients with colon cancer were
culturedwithVSL# 3medium.
Results:Probioticadministrationattenuateddevelopmentofsignsandsymptomsofcolitis,reducedcolonicexpressionof
TNFa,IL-6andIFNcandreservedcolonicdownregulationofPPARc,PXRandFXRcausedbyTNBS.Mesentericfatdepots
isolatedfromTNBS-treatedanimalshadincreasedexpressionofinflammatorymediatorsalongwithPPARc,FXR,leptinand
adiponectin.ThesechangeswerepreventedbyVSL#3.Creepingfatandmesentericadip
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