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dc.contributor.authorBhattacharyya, Sumit
dc.contributor.authorXue, Liquan
dc.contributor.authorDevkota, Suzanne
dc.contributor.authorChang, Eugene
dc.contributor.authorMorris, Stephan
dc.contributor.authorTobacman, Joanne K.
dc.date.accessioned2014-02-19T04:11:07Z
dc.date.available2014-02-19T04:11:07Z
dc.date.issued2013-05
dc.identifier.bibliographicCitationBhattacharyya, S., Xue, L. Q., Devkota, S., Chang, E. G., Morris, S. and Tobacman, J. K. Carrageenan-Induced Colonic Inflammation Is Reduced in Bcl10 Null Mice and Increased in IL-10-Deficient Mice. Mediators of Inflammation. 2013. DOI: 10.1155/2013/397642en_US
dc.identifier.issn0962-9351
dc.identifier.urihttp://hdl.handle.net/10027/11172
dc.descriptionCopyright © 2013 Sumit Bhattacharyya et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.en_US
dc.description.abstractThe common food additive carrageenan is a known activator of inflammation in mammalian tissues and stimulates both the canonical and noncanonical pathways of NF-kappa B activation. Exposure to low concentrations of carrageenan (10 mu g/mL in the water supply) has produced glucose intolerance, insulin resistance, and impaired insulin signaling in C57BL/6 mice. B-cell leukemia/lymphoma 10 (Bcl10) is a mediator of inflammatory signals from Toll-like receptor (TLR) 4 in myeloid and epithelial cells. Since the TLR4 signaling pathway is activated in diabetes and by carrageenan, we addressed systemic and intestinal inflammatory responses following carrageenan exposure in Bcl10 wild type, heterozygous, and null mice. Fecal calprotectin and circulating keratinocyte chemokine (KC), nuclear RelA and RelB, phospho(Thr559)-NF-kappa B-inducing kinase (NIK), and phospho(Ser36)-I kappa B alpha in the colonic epithelial cells were significantly less (P < 0.001) in the carrageenan-treated Bcl10 null mice than in controls. IL-10-deficient mice exposed to carrageenan in a germ-free environment showed an increase in activation of the canonical pathway of NF-kappa B (RelA) activation, but without increase in RelB or phospho-Bcl10, and exogenous IL-10 inhibited only the canonical pathway of NF-kappa B activation in cultured colonic cells. These findings demonstrate a Bcl10 requirement for maximum development of carrageenan-induced inflammation and lack of complete suppression by IL-10 of carrageenan-induced inflammation.en_US
dc.description.sponsorshipFunding was by Merit Review from the Veteran’s Administration to J. K. Tobacman and DDRCC (DK42086) and UH3 DK083993 to E. Chang for the support of the gnotobiotic facility.en_US
dc.language.isoen_USen_US
dc.publisherHindawi Publishing Corporationen_US
dc.subjectchemically induced disorderen_US
dc.subjectinflammationen_US
dc.subjectcarrageenanen_US
dc.subjectfood additiveen_US
dc.titleCarrageenan-Induced Colonic Inflammation Is Reduced in Bcl10 Null Mice and Increased in IL-10-Deficient Miceen_US
dc.typeArticleen_US


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