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All rights reserved. http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RARafVlUflJSY-LgBZ4GDST8P9PI-Io2Go0wWK7WIL2mY#_6 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RARafVlUflJSY-LgBZ4GDST8P9PI-Io2Go0wWK7WIL2mY#_5 http://www.w3.org/ns/prov#value The chemokine CCL28 is constitutively expressed by epithelial cells at several mucosal sites and is thought to function as a homeostatic chemoattractant of subpopulations of T cells and IgA B cells and to mediate antimicrobial activity. We report herein on the regulation of CCL28 in human colon epithelium by the proinflammatory cytokine IL-1, bacterial flagellin, and n-butyrate, a product of microbial metabolism. In vivo, CCL28 was markedly increased in the epithelium of pathologically inflamed compared with normal human colon. Human colon and small intestinal xenografts were used to model human intestinal epithelium in vivo. Xenografts constitutively expressed little, if any, CCL28 mRNA or protein. After stimulation with the proinflammatory cytokine IL-1, CCL28 mRNA and protein were significantly increased in the epithelium of colon but not small intestinal xenografts, although both upregulated the expression of another prototypic chemokine, CXCL8, in response to the identical stimulus. In studies of CCL28 regulation using human colon epithelial cell lines, proinflammatory stimuli, including IL-1, bacterial flagellin, and bacterial infection, significantly upregulated CCL28 mRNA expression and protein production. In addition, CCL28 mRNA expression and protein secretion by those cells were significantly increased by the short-chain fatty acid n-butyrate, and IL-1- or flagellin-stimulated upregulation of CCL28 by colon epithelial cells was synergistically increased by pretreatment of cells with n-butyrate. Consistent with its upregulated expression by proinflammatory stimuli, CCL28 mRNA expression was attenuated by pharmacological inhibitors of NF-kappaB activation. These findings indicate that CCL28 functions as an inflammatory chemokine in human colon epithelium and suggest the notion that CCL28 may act to counterregulate colonic inflammation. http://www.tkuhn.ch/bel2nanopub/RARafVlUflJSY-LgBZ4GDST8P9PI-Io2Go0wWK7WIL2mY#_5 http://www.w3.org/ns/prov#wasQuotedFrom http://www.ncbi.nlm.nih.gov/pubmed/15246961 http://www.tkuhn.ch/bel2nanopub/RARafVlUflJSY-LgBZ4GDST8P9PI-Io2Go0wWK7WIL2mY#_6 http://www.w3.org/2000/01/rdf-schema#label Selventa http://www.tkuhn.ch/bel2nanopub/RARafVlUflJSY-LgBZ4GDST8P9PI-Io2Go0wWK7WIL2mY#assertion http://www.w3.org/ns/prov#hadPrimarySource http://www.ncbi.nlm.nih.gov/pubmed/15246961 http://www.tkuhn.ch/bel2nanopub/RARafVlUflJSY-LgBZ4GDST8P9PI-Io2Go0wWK7WIL2mY#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://www.tkuhn.ch/bel2nanopub/RARafVlUflJSY-LgBZ4GDST8P9PI-Io2Go0wWK7WIL2mY#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://www.tkuhn.ch/bel2nanopub/RARafVlUflJSY-LgBZ4GDST8P9PI-Io2Go0wWK7WIL2mY#_5 http://www.tkuhn.ch/bel2nanopub/RARafVlUflJSY-LgBZ4GDST8P9PI-Io2Go0wWK7WIL2mY#pubinfo http://www.tkuhn.ch/bel2nanopub/RARafVlUflJSY-LgBZ4GDST8P9PI-Io2Go0wWK7WIL2mY http://purl.org/dc/terms/created 2014-07-03T14:32:25.688+02:00 http://www.tkuhn.ch/bel2nanopub/RARafVlUflJSY-LgBZ4GDST8P9PI-Io2Go0wWK7WIL2mY http://purl.org/pav/createdBy http://orcid.org/0000-0001-6818-334X http://www.tkuhn.ch/bel2nanopub/RARafVlUflJSY-LgBZ4GDST8P9PI-Io2Go0wWK7WIL2mY http://purl.org/pav/createdBy http://orcid.org/0000-0002-1267-0234