Publication:
Like will to like: abundances of closely related species can predict susceptibility to intestinal colonization by pathogenic and commensal bacteria

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dc.contributor.authorStecher, Bärbel
dc.contributor.authorChaffron, Samuel
dc.contributor.authorKäppeli, Rina
dc.contributor.authorHapfelmeier, Siegfried Hektor
dc.contributor.authorFreedrich, Susanne
dc.contributor.authorWeber, Thomas C
dc.contributor.authorKirundi, Jorum
dc.contributor.authorSuar, Mrutyunjay
dc.contributor.authorMcCoy, Kathy D
dc.contributor.authorvon Mering, Christian
dc.contributor.authorMacpherson, Andrew
dc.contributor.authorHardt, Wolf-Dietrich
dc.date.accessioned2024-10-10T20:43:46Z
dc.date.available2024-10-10T20:43:46Z
dc.date.issued2010
dc.description.abstractThe intestinal ecosystem is formed by a complex, yet highly characteristic microbial community. The parameters defining whether this community permits invasion of a new bacterial species are unclear. In particular, inhibition of enteropathogen infection by the gut microbiota ( = colonization resistance) is poorly understood. To analyze the mechanisms of microbiota-mediated protection from Salmonella enterica induced enterocolitis, we used a mouse infection model and large scale high-throughput pyrosequencing. In contrast to conventional mice (CON), mice with a gut microbiota of low complexity (LCM) were highly susceptible to S. enterica induced colonization and enterocolitis. Colonization resistance was partially restored in LCM-animals by co-housing with conventional mice for 21 days (LCM(con21)). 16S rRNA sequence analysis comparing LCM, LCM(con21) and CON gut microbiota revealed that gut microbiota complexity increased upon conventionalization and correlated with increased resistance to S. enterica infection. Comparative microbiota analysis of mice with varying degrees of colonization resistance allowed us to identify intestinal ecosystem characteristics associated with susceptibility to S. enterica infection. Moreover, this system enabled us to gain further insights into the general principles of gut ecosystem invasion by non-pathogenic, commensal bacteria. Mice harboring high commensal E. coli densities were more susceptible to S. enterica induced gut inflammation. Similarly, mice with high titers of Lactobacilli were more efficiently colonized by a commensal Lactobacillus reuteri(RR) strain after oral inoculation. Upon examination of 16S rRNA sequence data from 9 CON mice we found that closely related phylotypes generally display significantly correlated abundances (co-occurrence), more so than distantly related phylotypes. Thus, in essence, the presence of closely related species can increase the chance of invasion of newly incoming species into the gut ecosystem. We provide evidence that this principle might be of general validity for invasion of bacteria in preformed gut ecosystems. This might be of relevance for human enteropathogen infections as well as therapeutic use of probiotic commensal bacteria.
dc.description.sponsorshipUniversitätsklinik für Viszerale Chirurgie und Medizin, Gastroenterologie
dc.identifier.doi10.7892/boris.1484
dc.identifier.isi000274227100002
dc.identifier.pmid20062525
dc.identifier.publisherDOI10.1371/journal.ppat.1000711
dc.identifier.urihttps://boris-portal.unibe.ch/handle/20.500.12422/72201
dc.language.isoen
dc.publisherPublic Library of Science
dc.publisher.placeSan Francisco, Calif.
dc.relation.ispartofPLoS pathogens
dc.relation.issn1553-7366
dc.relation.organizationDCD5A442BB16E17DE0405C82790C4DE2
dc.titleLike will to like: abundances of closely related species can predict susceptibility to intestinal colonization by pathogenic and commensal bacteria
dc.typearticle
dspace.entity.typePublication
dspace.file.typetext
oaire.citation.issue1
oaire.citation.startPagee1000711
oaire.citation.volume6
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oairecerif.author.affiliationUniversitätsklinik für Viszerale Chirurgie und Medizin, Gastroenterologie
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oairecerif.author.affiliationUniversitätsklinik für Viszerale Chirurgie und Medizin, Gastroenterologie
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unibe.description.ispublishedpub
unibe.eprints.legacyId1484
unibe.journal.abbrevTitlePLOS PATHOG
unibe.refereedTRUE
unibe.subtype.articlejournal

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