Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pone.0022978
DC FieldValue
dc.titleProbiotics modulate intestinal expression of nuclear receptor and provide Counter-Regulatory signals to Inflammation-Driven adipose tissue activation
dc.contributor.authorMencarelli A.
dc.contributor.authorDistrutti E.
dc.contributor.authorRenga B.
dc.contributor.authorD'Amore C.
dc.contributor.authorCipriani S.
dc.contributor.authorPalladino G.
dc.contributor.authorDonini A.
dc.contributor.authorRicci P.
dc.contributor.authorFiorucci S.
dc.date.accessioned2019-11-11T08:38:40Z
dc.date.available2019-11-11T08:38:40Z
dc.date.issued2011
dc.identifier.citationMencarelli A., Distrutti E., Renga B., D'Amore C., Cipriani S., Palladino G., Donini A., Ricci P., Fiorucci S. (2011). Probiotics modulate intestinal expression of nuclear receptor and provide Counter-Regulatory signals to Inflammation-Driven adipose tissue activation. PLoS ONE 6 (7) : e22978. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0022978
dc.identifier.issn19326203
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/162037
dc.description.abstractBackground: 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-activated receptors (PPAR)-? and -?, pregnane x receptor (PXR), farnesoid x receptor (FXR) and liver x-receptor (LXR) are ligand-activated nuclear receptor that provide counter-regulatory signals to dysregulated immunity and modulates adipose tissue. Aims: To investigate the expression and function of nuclear receptors in intestinal and adipose tissues in a rodent model of colitis and mesenteric fat from Crohn's patients and to investigate their modulation by probiotics. 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 cultured with VSL#3 medium. Results: Probiotic administration attenuated development of signs and symptoms of colitis, reduced colonic expression of TNF?, IL-6 and IFN? and reserved colonic downregulation of PPAR?, PXR and FXR caused by TNBS. Mesenteric fat depots isolated from TNBS-treated animals had increased expression of inflammatory mediators along with PPAR?, FXR, leptin and adiponectin. These changes were prevented by VSL#3. Creeping fat and mesenteric adipose tissue from Crohn's patients showed a differential expression of PPAR? and FXR with both tissue expressing high levels of leptin. Exposure of these tissues to VSL#3 medium abrogates leptin release. Conclusions: Mesenteric adipose tissue from rodent colitis and Crohn's disease is metabolically active and shows inflammation-driven regulation of PPAR?, FXR and leptin. Probiotics correct the inflammation-driven metabolic dysfunction. © 2011 Mencarelli et al.
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20191101
dc.subjectadiponectin
dc.subjectcell nucleus receptor
dc.subjectciprofloxacin
dc.subjectfarnesoid X receptor
dc.subjectgamma interferon
dc.subjectinterleukin 6
dc.subjectleptin
dc.subjectliver X receptor
dc.subjectmetronidazole
dc.subjectperoxisome proliferator activated receptor alpha
dc.subjectperoxisome proliferator activated receptor gamma
dc.subjectpregnane X receptor
dc.subjectprobiotic agent
dc.subjecttumor necrosis factor alpha
dc.subjecttumor necrosis factor alpha inhibitor
dc.subjectVSL3
dc.subjectcell receptor
dc.subjectcytokine
dc.subjectfarnesoid X receptor
dc.subjectfarnesoid X-activated receptor
dc.subjectliver X receptor
dc.subjectmessenger RNA
dc.subjectorphan nuclear receptor
dc.subjectperoxisome proliferator activated receptor gamma
dc.subjectpregnane X receptor
dc.subjectprobiotic agent
dc.subjectsteroid receptor
dc.subjecttrinitrobenzenesulfonic acid
dc.subjectabdominal abscess
dc.subjectabdominal fat
dc.subjectadipose tissue
dc.subjectadult
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectantiinflammatory activity
dc.subjectarticle
dc.subjectclinical article
dc.subjectclinical feature
dc.subjectcolitis
dc.subjectcolon cancer
dc.subjectconcentration response
dc.subjectcontrolled study
dc.subjectCrohn disease
dc.subjectdisease course
dc.subjectenteritis
dc.subjectenzyme activation
dc.subjectfemale
dc.subjecthuman
dc.subjecthuman tissue
dc.subjectimmunomodulation
dc.subjectinflammation
dc.subjectintestine cell
dc.subjectintestine fistula
dc.subjectmale
dc.subjectmouse
dc.subjectnonhuman
dc.subjectprotein expression
dc.subjectprotein function
dc.subjectprotein localization
dc.subjectprotein secretion
dc.subjectregulatory mechanism
dc.subjectsignal transduction
dc.subjecttissue culture
dc.subjecttissue level
dc.subjecttreatment duration
dc.subjectanimal
dc.subjectcell culture
dc.subjectchemically induced disorder
dc.subjectcolitis
dc.subjectdrug effect
dc.subjectenzyme immunoassay
dc.subjectenzyme linked immunosorbent assay
dc.subjectgenetic transcription
dc.subjectgenetics
dc.subjectintestine
dc.subjectmesentery
dc.subjectmetabolism
dc.subjectpathology
dc.subjectpathophysiology
dc.subjectreverse transcription polymerase chain reaction
dc.subjectWestern blotting
dc.subjectAnimalia
dc.subjectMus
dc.subjectRodentia
dc.subjectAdipose Tissue
dc.subjectAdult
dc.subjectAnimals
dc.subjectBlotting, Western
dc.subjectCells, Cultured
dc.subjectColitis
dc.subjectCytokines
dc.subjectEnzyme-Linked Immunosorbent Assay
dc.subjectFemale
dc.subjectHumans
dc.subjectImmunoenzyme Techniques
dc.subjectInflammation
dc.subjectIntestines
dc.subjectMale
dc.subjectMesentery
dc.subjectMice
dc.subjectOrphan Nuclear Receptors
dc.subjectPPAR gamma
dc.subjectProbiotics
dc.subjectReceptors, Cytoplasmic and Nuclear
dc.subjectReceptors, Steroid
dc.subjectReverse Transcriptase Polymerase Chain Reaction
dc.subjectRNA, Messenger
dc.subjectSignal Transduction
dc.subjectTranscription, Genetic
dc.subjectTrinitrobenzenesulfonic Acid
dc.typeArticle
dc.contributor.departmentDEAN'S OFFICE (DUKE-NUS MEDICAL SCHOOL)
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.description.doi10.1371/journal.pone.0022978
dc.description.sourcetitlePLoS ONE
dc.description.volume6
dc.description.issue7
dc.description.pagee22978
dc.published.statePublished
Appears in Collections:Elements
Staff Publications

Show simple item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
10_1371_journal_pone_0022978.pdf2.31 MBAdobe PDF

OPEN

NoneView/Download

Google ScholarTM

Check

Altmetric


This item is licensed under a Creative Commons License Creative Commons