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dc.contributor.authorBerger, CN
dc.contributor.authorCrepin, VF
dc.contributor.authorRoumeliotis, TI
dc.contributor.authorWright, JC
dc.contributor.authorCarson, D
dc.contributor.authorPevsner-Fischer, M
dc.contributor.authorFurniss, RCD
dc.contributor.authorDougan, G
dc.contributor.authorDori-Bachash, M
dc.contributor.authorYu, L
dc.contributor.authorClements, A
dc.contributor.authorCollins, JW
dc.contributor.authorElinav, E
dc.contributor.authorLarrouy-Maumus, GJ
dc.contributor.authorChoudhary, JS
dc.contributor.authorFrankel, G
dc.date.accessioned2017-11-23T12:11:22Z
dc.date.issued2017-11-07
dc.identifier.citationCell metabolism, 2017, 26 (5), pp. 738 - 752.e6
dc.identifier.issn1550-4131
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/939
dc.identifier.eissn1932-7420
dc.identifier.doi10.1016/j.cmet.2017.09.003
dc.description.abstractThe intestinal epithelial cells (IECs) that line the gut form a robust line of defense against ingested pathogens. We investigated the impact of infection with the enteric pathogen Citrobacter rodentium on mouse IEC metabolism using global proteomic and targeted metabolomics and lipidomics. The major signatures of the infection were upregulation of the sugar transporter Sglt4, aerobic glycolysis, and production of phosphocreatine, which mobilizes cytosolic energy. In contrast, biogenesis of mitochondrial cardiolipins, essential for ATP production, was inhibited, which coincided with increased levels of mucosal O2 and a reduction in colon-associated anaerobic commensals. In addition, IECs responded to infection by activating Srebp2 and the cholesterol biosynthetic pathway. Unexpectedly, infected IECs also upregulated the cholesterol efflux proteins AbcA1, AbcG8, and ApoA1, resulting in higher levels of fecal cholesterol and a bloom of Proteobacteria. These results suggest that C. rodentium manipulates host metabolism to evade innate immune responses and establish a favorable gut ecosystem.
dc.formatPrint-Electronic
dc.format.extent738 - 752.e6
dc.languageeng
dc.language.isoeng
dc.publisherCELL PRESS
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.subjectIntestinal Mucosa
dc.subjectCell Line
dc.subjectMitochondria
dc.subjectEpithelial Cells
dc.subjectFeces
dc.subjectAnimals
dc.subjectMice, Inbred C3H
dc.subjectMice, Inbred C57BL
dc.subjectHumans
dc.subjectMice
dc.subjectCitrobacter rodentium
dc.subjectCholesterol
dc.subjectAdenosine Triphosphate
dc.subjectProteomics
dc.subjectFemale
dc.subjectMale
dc.subjectImmunity, Innate
dc.subjectMetabolomics
dc.titleCitrobacter rodentium Subverts ATP Flux and Cholesterol Homeostasis in Intestinal Epithelial Cells In Vivo.
dc.typeJournal Article
dcterms.dateAccepted2017-09-06
rioxxterms.versionofrecord10.1016/j.cmet.2017.09.003
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0
rioxxterms.licenseref.startdate2017-11
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfCell metabolism
pubs.issue5
pubs.notes6 months
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology/Functional Proteomics Group
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology/Functional Proteomics Group
pubs.publication-statusPublished
pubs.volume26
pubs.embargo.terms6 months
icr.researchteamFunctional Proteomics Group
dc.contributor.icrauthorRoumeliotis, Theodoros
dc.contributor.icrauthorWright, James
dc.contributor.icrauthorChoudhary, Jyoti


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