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dc.contributor.authorDanne, Camille
dc.contributor.authorRyzhakov, Grigory
dc.contributor.authorMartinez-Lopez, Maria 
dc.contributor.authorIlott, Nicholas Edward
dc.contributor.authorFranchini, Fanny
dc.contributor.authorCuskin, Fiona
dc.contributor.authorLowe, Elisabeth C
dc.contributor.authorBullers, Samuel J
dc.contributor.authorArthur, J Simon C
dc.contributor.authorPowrie, Fiona
dc.date.accessioned2019-03-11T08:52:41Z
dc.date.available2019-03-11T08:52:41Z
dc.date.issued2017-12-13
dc.identifier.citationCell Host Microbe. 2017; 22(6):733-745es_ES
dc.identifier.issn1931-3128es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/7310
dc.description.abstractInteractions between the host and its microbiota are of mutual benefit and promote health. Complex molecular pathways underlie this dialog, but the identity of microbe-derived molecules that mediate the mutualistic state remains elusive. Helicobacter hepaticus is a member of the mouse intestinal microbiota that is tolerated by the host. In the absence of an intact IL-10 signaling, H. hepaticus induces an IL-23-driven inflammatory response in the intestine. Here we investigate the interactions between H. hepaticus and host immune cells that may promote mutualism, and the microbe-derived molecule(s) involved. Our results show that H. hepaticus triggers early IL-10 induction in intestinal macrophages and produces a large soluble polysaccharide that activates a specific MSK/CREB-dependent anti-inflammatory and repair gene signature via the receptor TLR2. These data identify a host-bacterial interaction that promotes mutualistic mechanisms at the intestinal interface. Further understanding of this pathway may provide novel prevention and treatment strategies for inflammatory bowel disease.es_ES
dc.description.sponsorshipWe thank the High-Throughput Genomics Group at the Wellcome Trust Centre for Human Genetics for the generation of the Sequencing data. F.F. was supported by Cancer Research UK (OCRC-DPhil13-FF) and N.E.I. by the Kennedy Trust (KENN 15 16 03). M.M.-L. received a fellowship from the Spanish Ministry of Education, Culture, and Sport. This work was funded by the Wellcome Trust UK (095688/Z/11/Z), an ERC grant (Advanced Grant Ares(2013)3687660), and the Fondation Louis Jeantetes_ES
dc.language.isoenges_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectCREBes_ES
dc.subjectHelicobacter hepaticuses_ES
dc.subjectMSK1/2es_ES
dc.subjectTLR2es_ES
dc.subjectanti-inflammatory gene signaturees_ES
dc.subjecthost-microbe interactionses_ES
dc.subjectinflammatory bowel diseasees_ES
dc.subjectmacrophagees_ES
dc.subjectmutualismes_ES
dc.subjectpolysaccharidees_ES
dc.subject.meshAnimals es_ES
dc.subject.meshHelicobacter hepaticus es_ES
dc.subject.meshImmunosuppressive Agents es_ES
dc.subject.meshInterleukin-10 es_ES
dc.subject.meshInterleukin-23 es_ES
dc.subject.meshMacrophages es_ES
dc.subject.meshMice es_ES
dc.subject.meshPolysaccharides, Bacterial es_ES
dc.subject.meshToll-Like Receptor 2 es_ES
dc.subject.meshSymbiosis es_ES
dc.titleA Large Polysaccharide Produced by Helicobacter hepaticus Induces an Anti-inflammatory Gene Signature in Macrophageses_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID29241040es_ES
dc.format.volume22es_ES
dc.format.number6es_ES
dc.format.page733-745.e5es_ES
dc.identifier.doi10.1016/j.chom.2017.11.002es_ES
dc.contributor.funderMinisterio de Educación y Ciencia (España)es_ES
dc.contributor.funderWellcome Trustes_ES
dc.contributor.funderKennedy Trustes_ES
dc.contributor.funderFoundation Lous Jeantetes_ES
dc.contributor.funderEuropean Commissiones_ES
dc.contributor.funderEuropean Research Counciles_ES
dc.description.peerreviewedes_ES
dc.identifier.e-issn1934-6069es_ES
dc.identifier.journalCell host & microbees_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Inmunobiologíaes_ES
dc.repisalud.institucionCNICes_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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