Please use this identifier to cite or link to this item: https://doi.org/10.1186/s12866-016-0624-8
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dc.titleCaenorhabditis elegans susceptibility to gut Enterococcus faecalis infection is associated with fat metabolism and epithelial junction integrity
dc.contributor.authorSim, S
dc.contributor.authorHibberd, M.L
dc.date.accessioned2020-10-27T10:48:05Z
dc.date.available2020-10-27T10:48:05Z
dc.date.issued2016
dc.identifier.citationSim, S, Hibberd, M.L (2016). Caenorhabditis elegans susceptibility to gut Enterococcus faecalis infection is associated with fat metabolism and epithelial junction integrity. BMC Microbiology 16 (1) : 624. ScholarBank@NUS Repository. https://doi.org/10.1186/s12866-016-0624-8
dc.identifier.issn14712180
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/181397
dc.description.abstractBackground: Gut bacteria-host interactions have been implicated in the pathogenesis of numerous human diseases, but few mechanisms have been described. The genetically tractable nematode worm Caenorhabditis elegans can be infected with pathogenic bacteria, such as the human gut commensal Enterococcus faecalis, via feeding, making it a good model for studying these interactions. Results: An RNAi screen of 17 worm candidate genes revealed that knockdown of the transcription factor nhr-49, a master regulator of fat metabolism, shortens worm lifespan upon infection with E. faecalis (and other potentially pathogenic bacteria) compared to Escherichia coli. The functional similarity of nhr-49 to the mammalian peroxisome proliferator-activated receptors (PPARs) suggests that this is mediated through a link between fatty acid metabolism and innate immunity. In addition, knockdown of either dlg-1 or ajm-1, which encode physically interacting proteins in the C. elegans epithelial junction, also reduces worm lifespan upon E. faecalis challenge, demonstrating the importance of the intestinal epithelium as an immune barrier. Conclusions: The protective roles identified for nhr-49, dlg-1, and ajm-1 suggest mechanistic interactions between the gut microbiota, host fatty acid metabolism, innate immunity, and epithelial junction integrity that are remarkably similar to those implicated in human metabolic and inflammatory diseases. © 2016 Sim and Hibberd.
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjectfat
dc.subjectfatty acid
dc.subjectperoxisome proliferator activated receptor
dc.subjecttranscription factor
dc.subjectCaenorhabditis elegans protein
dc.subjectfat
dc.subjectajm 1 gene
dc.subjectArticle
dc.subjectCaenorhabditis elegans
dc.subjectcontrolled study
dc.subjectdlg 1 gene
dc.subjectenterococcal infection
dc.subjectEnterococcus faecalis
dc.subjectEscherichia coli
dc.subjectfatty acid metabolism
dc.subjectgene
dc.subjectgene function
dc.subjectgene silencing
dc.subjectinfection sensitivity
dc.subjectinnate immunity
dc.subjectintestine epithelium
dc.subjectintestine epithelium junction
dc.subjectintestine flora
dc.subjectlifespan
dc.subjectlipid metabolism
dc.subjectnhr 49 gene
dc.subjectnonhuman
dc.subjectprotection
dc.subjectRNA interference
dc.subjectanimal
dc.subjectCaenorhabditis elegans
dc.subjectdisease model
dc.subjectEnterococcus faecalis
dc.subjectfemale
dc.subjectgenetics
dc.subjectGram positive infection
dc.subjecthost pathogen interaction
dc.subjecthuman
dc.subjectintestine mucosa
dc.subjectmale
dc.subjectmetabolism
dc.subjectmicrobiology
dc.subjectphysiology
dc.subjectAnimals
dc.subjectCaenorhabditis elegans
dc.subjectCaenorhabditis elegans Proteins
dc.subjectDisease Models, Animal
dc.subjectEnterococcus faecalis
dc.subjectFats
dc.subjectFemale
dc.subjectGastrointestinal Microbiome
dc.subjectGram-Positive Bacterial Infections
dc.subjectHost-Pathogen Interactions
dc.subjectHumans
dc.subjectIntestinal Mucosa
dc.subjectMale
dc.typeArticle
dc.contributor.departmentSAW SWEE HOCK SCHOOL OF PUBLIC HEALTH
dc.description.doi10.1186/s12866-016-0624-8
dc.description.sourcetitleBMC Microbiology
dc.description.volume16
dc.description.issue1
dc.description.page624
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