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dc.contributor.authorAl-Hassi, Hafid O.-
dc.contributor.authorMann, Elizabeth R.-
dc.contributor.authorFernández-Salazar, Luis-
dc.contributor.authorGarrote, José Antonio-
dc.contributor.authorArranz, Eduardo-
dc.contributor.authorMargolles Barros, Abelardo-
dc.contributor.authorKnight, Stella C.-
dc.contributor.authorBernardo, David-
dc.date.accessioned2015-06-19T13:06:32Z-
dc.date.available2015-06-19T13:06:32Z-
dc.date.issued2014-
dc.identifierdoi: 10.1002/mnfr.201300596-
dc.identifierissn: 1613-4125-
dc.identifiere-issn: 1613-4133-
dc.identifier.citationMolecular Nutrition and Food Research 58(5): 1132-1143 (2014)-
dc.identifier.urihttp://hdl.handle.net/10261/116904-
dc.descriptionThis is an open access article under the terms of the Creative Commons Attribution License.-- et al.-
dc.description.abstract[Scope]: The human/microbiota cross-talk is partially mediated by bacteria-derived peptides like Serine-Threonine peptide (STp), which is resistant to gut proteolysis, is found in the human healthy colon and induces regulatory properties on gut dendritic cells (DCs); here we characterized human gut DC in ulcerative colitis (UC) patients and studied the effect of STp on their properties. [Methods and results]: Human colonic DC from healthy controls and UC patients were isolated, conditioned for 24 h +/- STp and characterized by flow cytometry, immunohistochemistry, and electron microscopy. Expression of immature DC markers DC-SIGN and ILT3, and Toll-like receptors were increased on gut UC-DC. Langerin (involved in phagocytosis), lymph node homing marker CCR7, and activation markers CD40/CD80/CD86 were decreased in UC. Gut DC had restricted stimulatory capacity for T-cells in UC. Conditioning of DC with STp in vitro reduced Toll-like receptor expression, increased CD40 and CD80 expression, and restored their stimulatory capacity. [Conclusion]: Colonic DCs display an abnormal immature phenotype in UC, which was partially restored following STp treatment. Bacteria-derived metabolites, like STp, seem to have a role in gut homeostasis that is missing in UC so they might lead a new era of probiotic products setting the basis for nondrug dietary therapy in inflammatory bowel disease. © 2013 The Authors. Molecular Nutrition & Food Research published by Wiley-VCH Verlag GmbH & Co. KGaA Weinheim.-
dc.description.sponsorshipThe author(s) gratefully acknowledge the support of the Biotechnology and Biological Sciences Research Council (BBSRC), this research was funded by the BBSRC Institute Strategic Programme for Gut Health and Food Safety BB/J004529/1. The authors also thank the St Mark’s Hospital Foundation, The Association for International Cancer Research (AICR), Scotland, and the Junta de Castilla y León (GRS175/B/07).-
dc.publisherJohn Wiley & Sons-
dc.relation.isversionofPublisher's version-
dc.rightsopenAccess-
dc.subjectMicrobiota-
dc.subjectPostbiotics-
dc.subjectSTp-
dc.subjectUlcerative colitis-
dc.subjectDendritic cells-
dc.titleAltered human gut dendritic cell properties in ulcerative colitis are reversed by Lactobacillus plantarum extracellular encrypted peptide STp-
dc.typeArtículo-
dc.identifier.doi10.1002/mnfr.201300596-
dc.relation.publisherversionhttp://dx.doi.org/10.1002/mnfr.201300596-
dc.date.updated2015-06-19T13:06:32Z-
dc.description.versionPeer Reviewed-
dc.language.rfc3066eng-
dc.rights.licensehttp://creativecommons.org/licenses/by/3.0/-
dc.contributor.funderBiotechnology and Biological Sciences Research Council (UK)-
dc.contributor.funderSt. Mark's Hospital Foundation-
dc.contributor.funderAssociation for International Cancer Research-
dc.contributor.funderJunta de Castilla y León-
dc.relation.csic-
dc.identifier.funderhttp://dx.doi.org/10.13039/501100000268es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/100004435es_ES
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