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dc.contributor.authorCardoso, Ana
dc.contributor.authorGil Castro, Antonio
dc.contributor.authorMartins, Ana Catarina
dc.contributor.authorCarriche, Guilhermina M
dc.contributor.authorMurigneux, Valentine
dc.contributor.authorCastro, Isabel
dc.contributor.authorCumano, Ana
dc.contributor.authorVieira, Paulo
dc.contributor.authorSaraiva, Margarida
dc.date.accessioned2020-06-16T09:47:18Z
dc.date.available2020-06-16T09:47:18Z
dc.date.issued2018-03-01
dc.identifier.citationFront Immunol. 2018;9:400. Published 2018 Mar 1. doi:10.3389/fimmu.2018.00400.en_US
dc.identifier.issn1664-3224
dc.identifier.pmid29545807
dc.identifier.doi10.3389/fimmu.2018.00400
dc.identifier.urihttp://hdl.handle.net/10033/622299
dc.description.abstractInflammatory bowel disease encompasses a group of chronic-inflammatory conditions of the colon and small intestine. These conditions are characterized by exacerbated inflammation of the organ that greatly affects the quality of life of patients. Molecular mechanisms counteracting this hyperinflammatory status of the gut offer strategies for therapeutic intervention. Among these regulatory molecules is the anti-inflammatory cytokine interleukin (IL)-10, as shown in mice and humans. Indeed, IL-10 signaling, particularly in macrophages, is essential for intestinal homeostasis. We sought to investigate the temporal profile of IL-10-mediated protection during chemical colitis and which were the underlying mechanisms. Using a novel mouse model of inducible IL-10 overexpression (pMT-10), described here, we show that mice preconditioned with IL-10 for 8 days before dextran sulfate sodium (DSS) administration developed a milder colitic phenotype. In IL-10-induced colitic mice, Ly6C cells isolated from the lamina propria showed a decreased inflammatory profile. Because our mouse model leads to transcription of the IL-10 transgene in the bone marrow and elevated seric IL-10 concentration, we investigated whether IL-10 could imprint immune cells in a long-lasting way, thus conferring sustained protection to colitis. We show that this was not the case, as IL-10-afforded protection was only observed if IL-10 induction immediately preceded DSS-mediated colitis. Thus, despite the protection afforded by IL-10 in colitis, novel strategies are required, specifically to achieve long-lasting protection.en_US
dc.language.isoenen_US
dc.publisherFrontiersen_US
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectcolitisen_US
dc.subjectinflammationen_US
dc.subjectinterleukin-10en_US
dc.subjectmacrophagesen_US
dc.subjecttherapyen_US
dc.titleThe Dynamics of Interleukin-10-Afforded Protection during Dextran Sulfate Sodium-Induced Colitis.en_US
dc.typeArticleen_US
dc.typeOtheren_US
dc.contributor.departmentTWINCORE, Zentrum für experimentelle und klinische Infektionsforschung GmbH,Feodor-Lynen Str. 7, 30625 Hannover, Germany.en_US
dc.identifier.journalFrontiers in immunologyen_US
dc.source.volume9
dc.source.beginpage400
dc.source.endpage
refterms.dateFOA2020-06-16T09:47:19Z
dc.source.journaltitleFrontiers in immunology
dc.source.countrySwitzerland


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