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Klebsiella michiganensis transmission enhances resistance to Enterobacteriaceae gut invasion by nutrition competition

2020-01-20Journal article Open access
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dc.contributor.authorOliveira, Rita A
dc.contributor.authorNg, Katharine M
dc.contributor.authorCorreia, Margarida B
dc.contributor.authorCabral, Vitor
dc.contributor.authorShi, Handuo
dc.contributor.authorSonnenburg, Justin L
dc.contributor.authorHuang, Kerwyn Casey
dc.contributor.authorXavier, Karina B
dc.date.accessioned2020-03-17T11:02:24Z
dc.date.available2020-03-17T11:02:24Z
dc.date.issued2020-01-20
dc.description.abstractIntestinal microbiotas contain beneficial microorganisms that protect against pathogen colonization; treatment with antibiotics disrupts the microbiota and compromises colonization resistance. Here, we determine the impact of exchanging microorganisms between hosts on resilience to the colonization of invaders after antibiotic-induced dysbiosis. We assess the functional consequences of dysbiosis using a mouse model of colonization resistance against Escherichia coli. Antibiotics caused stochastic loss of members of the microbiota, but the microbiotas of co-housed mice remained more similar to each other compared with the microbiotas among singly housed animals. Strikingly, co-housed mice maintained colonization resistance after treatment with antibiotics, whereas most singly housed mice were susceptible to E. coli. The ability to retain or share the commensal Klebsiella michiganensis, a member of the Enterobacteriaceae family, was sufficient for colonization resistance after treatment with antibiotics. K. michiganensis generally outcompeted E. coli in vitro, but in vivo administration of galactitol-a nutrient that supports the growth of only E. coli-to bi-colonized gnotobiotic mice abolished the colonization-resistance capacity of K. michiganensis against E. coli, supporting the idea that nutrient competition is the primary interaction mechanism. K. michiganensis also hampered colonization of the pathogen Salmonella, prolonging host survival. Our results address functional consequences of the stochastic effects of microbiota perturbations, whereby microbial transmission through host interactions can facilitate reacquisition of beneficial commensals, minimizing the negative impact of antibiotics.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.doi10.1038/s41564-019-0658-4pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.7/940
dc.language.isoengpt_PT
dc.peerreviewednopt_PT
dc.publisherNature Researchpt_PT
dc.relationFCTpt_PT
dc.relation.publisherversionhttps://www.nature.com/articles/s41564-019-0658-4pt_PT
dc.subjectEscherichia colipt_PT
dc.subjectKlebsiella michiganensispt_PT
dc.subjectSalmonella Typhimuriumpt_PT
dc.subjectProteobacteriapt_PT
dc.subjectStreptomycinpt_PT
dc.subjectCiprofloxacinpt_PT
dc.subjectHousingpt_PT
dc.subjectGamma diversitypt_PT
dc.subjectNutrient competitionpt_PT
dc.subjectMicrobiotapt_PT
dc.subjectDysbiosispt_PT
dc.titleKlebsiella michiganensis transmission enhances resistance to Enterobacteriaceae gut invasion by nutrition competitionpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.titleNature microbiologypt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT

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