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dc.contributor.authorvan de Wouw, Marcel
dc.contributor.authorWalsh, Aaron M.
dc.contributor.authorCrispie, Fiona
dc.contributor.authorvan Leuven, Lucas
dc.contributor.authorLyte, Joshua M
dc.contributor.authorBoehme, Marcus
dc.contributor.authorClarke, Gerard
dc.contributor.authorDinan, Timothy G
dc.contributor.authorCotter, Paul D.
dc.contributor.authorCryan, John F
dc.date.accessioned2020-07-08T16:28:41Z
dc.date.available2020-07-08T16:28:41Z
dc.date.issued2020-05-18
dc.identifier.citationvan de Wouw, M., Walsh, A.M., Crispie, F. et al. Distinct actions of the fermented beverage kefir on host behaviour, immunity and microbiome gut-brain modules in the mouse. Microbiome 8, 67 (2020). https://doi.org/10.1186/s40168-020-00846-5en_US
dc.identifier.urihttps://doi.org/10.1186/s40168-020-00846-5
dc.identifier.urihttp://hdl.handle.net/11019/2165
dc.descriptionpeer-revieweden_US
dc.description.abstractBackground Mounting evidence suggests a role for the gut microbiota in modulating brain physiology and behaviour, through bi-directional communication, along the gut-brain axis. As such, the gut microbiota represents a potential therapeutic target for influencing centrally mediated events and host behaviour. It is thus notable that the fermented milk beverage kefir has recently been shown to modulate the composition of the gut microbiota in mice. It is unclear whether kefirs have differential effects on microbiota-gut-brain axis and whether they can modulate host behaviour per se. Methods To address this, two distinct kefirs (Fr1 and UK4), or unfermented milk control, were administered to mice that underwent a battery of tests to characterise their behavioural phenotype. In addition, shotgun metagenomic sequencing of ileal, caecal and faecal matter was performed, as was faecal metabolome analysis. Finally, systemic immunity measures and gut serotonin levels were assessed. Statistical analyses were performed by ANOVA followed by Dunnett's post hoc test or Kruskal-Wallis test followed by Mann-Whitney U test. Results Fr1 ameliorated the stress-induced decrease in serotonergic signalling in the colon and reward-seeking behaviour in the saccharin preference test. On the other hand, UK4 decreased repetitive behaviour and ameliorated stress-induced deficits in reward-seeking behaviour. Furthermore, UK4 increased fear-dependent contextual memory, yet decreased milk gavage-induced improvements in long-term spatial learning. In the peripheral immune system, UK4 increased the prevalence of Treg cells and interleukin 10 levels, whereas Fr1 ameliorated the milk gavage stress-induced elevation in neutrophil levels and CXCL1 levels. Analysis of the gut microbiota revealed that both kefirs significantly changed the composition and functional capacity of the host microbiota, where specific bacterial species were changed in a kefir-dependent manner. Furthermore, both kefirs increased the capacity of the gut microbiota to produce GABA, which was linked to an increased prevalence in Lactobacillus reuteri. Conclusions Altogether, these data show that kefir can signal through the microbiota-gut-immune-brain axis and modulate host behaviour. In addition, different kefirs may direct the microbiota toward distinct immunological and behavioural modulatory effects. These results indicate that kefir can positively modulate specific aspects of the microbiota-gut-brain axis and support the broadening of the definition of psychobiotic to include kefir fermented foods. Video abstract.en_US
dc.language.isoenen_US
dc.publisherBiomed Centralen_US
dc.relation.ispartofseriesMicrobiome;
dc.subjectMicrobiotaen_US
dc.subjectKefiren_US
dc.subjectMouseen_US
dc.subjectBrainen_US
dc.subjectBehaviouren_US
dc.subjectGABAen_US
dc.subjectImmunityen_US
dc.subjectSerotoninen_US
dc.subjectRewarden_US
dc.subjectLactobacillusen_US
dc.titleDistinct actions of the fermented beverage kefir on host behaviour, immunity and microbiome gut-brain modules in the mouseen_US
dc.typeArticleen_US
dc.date.updated2020-05-24T04:47:05Z
dc.language.rfc3066en
dc.rights.holderThe Author(s)
dc.identifier.doihttps://doi.org/10.1186/s40168-020-00846-5
dc.contributor.sponsorScience Foundation Irelanden_US
dc.contributor.sponsorGrantNumberSFI/12/RC/2273en_US
dc.contributor.sponsorGrantNumber(15/JPHDHL/3270en_US
refterms.dateFOA2020-07-08T16:28:41Z


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