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dc.contributor.authorBushell, Kristen N.en_US
dc.contributor.authorLeeman, Susan E.en_US
dc.contributor.authorGillespie, Earlen_US
dc.contributor.authorGower, Adam C.en_US
dc.contributor.authorReed, Karen L.en_US
dc.contributor.authorStucchi, Arthur F.en_US
dc.contributor.authorBecker, James M.en_US
dc.contributor.authorAmar, Salomonen_US
dc.coverage.spatialUnited Statesen_US
dc.identifier.citationKristen N. Bushell, Susan E. Leeman, Earl Gillespie, Adam C. Gower, Karen L. Reed, Arthur F. Stucchi, James M. Becker, Salomon Amar. 2011. "LITAF mediation of increased TNF-α secretion from inflamed colonic lamina propria macrophages.." PLoS One, Volume 6, Issue 9,
dc.description.abstractDysregulation of TNF-α in lamina propria macrophages (LPM) is a feature of inflammatory bowel diseases (IBD). LPS-Induced-TNF-Alpha-Factor (LITAF) is a transcription factor that mediates TNF-α expression. To determine whether LITAF participates in the mediation of TNF-α expression in acutely inflamed colonic tissues, we first established the TNBS-induced colonic inflammation model in C57BL/6 mice. LPM were harvested from non-inflamed and inflamed colonic tissue and inflammatory parameters TNF-α and LITAF mRNA and protein levels were measured ex-vivo. LPM from TNBS-treated mice secreted significantly more TNF-α at basal state and in response to LPS than LPM from untreated mice (p<0.05). LITAF mRNA and protein levels were elevated in LPM from TNBS compared with untreated animals and LPS further increased LITAF protein levels in LPM from inflamed tissue (P<0.05). To further confirm the role of LITAF in acutely inflamed colonic tissues, TNBS-induced colonic inflammation was produced in LITAF macrophage specific knockout mice (LITAF mac -/- mice) and compared to wild type (WT) C57BL/6. Twenty four hours following TNBS administration, colonic tissue from LITAF mac -/- mice had less MPO activity and reduced colonic TNF-α mRNA then WT C57BL/6 mice (p<0.05). LPM harvested from LITAF mac -/- secreted significantly less TNF-α in response to LPS than wild type (WT) C57BL/6 (p<0.05). This study provides evidence that LITAF contributes to the regulation of TNF-α in LPM harvested following acute inflammation or LPS treatment paving the way for future work focusing on LITAF inhibitors in the treatment of TNF-α-mediated inflammatory conditions.en_US
dc.description.sponsorshipR01 DE014079 - NIDCR NIH HHS; R01 DE 014079 SA - NIDCR NIH HHSen_US
dc.relation.ispartofPLoS One
dc.subjectBlotting, westernen_US
dc.subjectDNA-binding proteinsen_US
dc.subjectEnzyme-linked immunosorbent assayen_US
dc.subjectMice, inbred C57BLen_US
dc.subjectMucous membraneen_US
dc.subjectNuclear proteinsen_US
dc.subjectReverse transcriptase polymerase chain reactionen_US
dc.subjectTranscription factorsen_US
dc.subjectTumor necrosis factor-alphaen_US
dc.subjectGeneral science & technologyen_US
dc.titleLITAF mediation of increased TNF-α secretion from inflamed colonic lamina propria macrophages.en_US
dc.description.versionPublished versionen_US
pubs.notesEmbargo: Not knownen_US
pubs.organisational-groupBoston Universityen_US
pubs.organisational-groupBoston University, College of Arts & Sciencesen_US
pubs.organisational-groupBoston University, School of Medicineen_US
atmire.atmiredoc.conversiontool© 2011 Bushell et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US

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