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IL-22 controls iron-dependent nutritional immunity against systemic bacterial infections

2017-02-03Journal article Open access
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dc.contributor.authorSakamoto, Kei
dc.contributor.authorKim, Yun-Gi
dc.contributor.authorHara, Hideki
dc.contributor.authorKamada, Nobuhiko
dc.contributor.authorCaballero-Flores, Gustavo
dc.contributor.authorTolosano, Emanuela
dc.contributor.authorSoares, Miguel P.
dc.contributor.authorPuente, José L.
dc.contributor.authorInohara, Naohiro
dc.contributor.authorNúñez, Gabriel
dc.date.accessioned2017-06-21T19:13:05Z
dc.date.available2018-02-01T01:30:09Z
dc.date.issued2017-02-03
dc.descriptionThis publication hasn't any creative commons license associated.pt_PT
dc.descriptionThis publication has a exclusive licensee of the American Association for the Advancement of Science.pt_PT
dc.descriptionThe deposited article contains attached the supplementary materials.pt_PT
dc.description.abstractHost immunity limits iron availability to pathogenic bacteria, but whether immunity limits pathogenic bacteria from accessing host heme, the major source of iron in the body, remains unclear. Using Citrobacter rodentium, a mouse enteric pathogen and Escherichia coli, a major cause of sepsis in humans as models, we find that interleukin-22, a cytokine best known for its ability to promote epithelial barrier function, also suppresses the systemic growth of bacteria by limiting iron availability to the pathogen. Using an unbiased proteomic approach to understand the mechanistic basis of IL-22 dependent iron retention in the host, we have identified that IL-22 induces the production of the plasma hemoglobin scavenger haptoglobin and heme scavenger hemopexin. Moreover, the anti-microbial effect of IL-22 depends on the induction of hemopexin expression, while haptogloblin is dispensable. Impaired pathogen clearance in infected Il22(-/-) mice was restored by administration and hemopexin-deficient mice had increased pathogen loads after infection. These studies reveal a previously unrecognized host defense mechanism regulated by IL-22 that relies on the induction of hemopexin to limit heme availability to bacteria leading to suppression of bacterial growth during systemic infections.pt_PT
dc.description.sponsorshipJapan Society for the Promotion of Science fellowship; Kanae Foundation for the Promotion of Medical Science; Mishima Kaiun Memorial Foundation; Consejo Nacional de Ciencia y Tecnología of Mexico post-doctoral fellowship: (454848); NIH grants: (DK091191, DK095782); Fundação Calouste Gulbenkian;pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationK. Sakamoto, Y.-G. Kim, H. Hara, N. Kamada, G. Caballero-Flores, E. Tolosano, M. P. Soares, J. L. Puente, N. Inohara, G. Núñez, IL-22 controls iron-dependent nutritional immunity against systemic bacterial infections. Sci. Immunol. 2(8) , eaai8371 (2017).pt_PT
dc.identifier.doi10.1126/sciimmunol.aai8371pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.7/766
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherNature Publishing Grouppt_PT
dc.relationJapan Society for the Promotion of Science fellowship (Research Abroad)pt_PT
dc.relationONACYT - 454848pt_PT
dc.relationTissue Damage Control Regulates The Pathogenesis of Immune Mediated Inflammatory Diseases
dc.relationNIH - DK095782pt_PT
dc.relation.publisherversionhttp://immunology.sciencemag.org/content/2/8/eaai8371/tab-pdfpt_PT
dc.subjectIL-22pt_PT
dc.subjectImmunitypt_PT
dc.subjectInfectious diseasept_PT
dc.subjectBacteriapt_PT
dc.subjectHemopexinpt_PT
dc.titleIL-22 controls iron-dependent nutritional immunity against systemic bacterial infectionspt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleTissue Damage Control Regulates The Pathogenesis of Immune Mediated Inflammatory Diseases
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/3599-PPCDT/PTDC%2FSAU-TOX%2F116627%2F2010/PT
oaire.awardURIinfo:eu-repo/grantAgreement/EC/FP7/294709/EU
oaire.citation.endPage9pt_PT
oaire.citation.issue8pt_PT
oaire.citation.startPage1pt_PT
oaire.citation.titleScience Immunologypt_PT
oaire.citation.volume2pt_PT
oaire.fundingStream3599-PPCDT
oaire.fundingStreamFP7
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100008530
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameEuropean Commission
rcaap.rightsembargoedAccesspt_PT
rcaap.typearticlept_PT
relation.isProjectOfPublication72d8fa6f-1215-4a61-bc70-515eef334d45
relation.isProjectOfPublication370f9aad-c4ef-4e35-b754-edc840dc6b5e
relation.isProjectOfPublication.latestForDiscovery370f9aad-c4ef-4e35-b754-edc840dc6b5e

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