Please use this identifier to cite or link to this item: https://doi.org/10.1186/s12866-016-0624-8
Title: Caenorhabditis elegans susceptibility to gut Enterococcus faecalis infection is associated with fat metabolism and epithelial junction integrity
Authors: Sim, S
Hibberd, M.L 
Keywords: fat
fatty acid
peroxisome proliferator activated receptor
transcription factor
Caenorhabditis elegans protein
fat
ajm 1 gene
Article
Caenorhabditis elegans
controlled study
dlg 1 gene
enterococcal infection
Enterococcus faecalis
Escherichia coli
fatty acid metabolism
gene
gene function
gene silencing
infection sensitivity
innate immunity
intestine epithelium
intestine epithelium junction
intestine flora
lifespan
lipid metabolism
nhr 49 gene
nonhuman
protection
RNA interference
animal
Caenorhabditis elegans
disease model
Enterococcus faecalis
female
genetics
Gram positive infection
host pathogen interaction
human
intestine mucosa
male
metabolism
microbiology
physiology
Animals
Caenorhabditis elegans
Caenorhabditis elegans Proteins
Disease Models, Animal
Enterococcus faecalis
Fats
Female
Gastrointestinal Microbiome
Gram-Positive Bacterial Infections
Host-Pathogen Interactions
Humans
Intestinal Mucosa
Male
Issue Date: 2016
Citation: Sim, 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
Rights: Attribution 4.0 International
Abstract: Background: 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.
Source Title: BMC Microbiology
URI: https://scholarbank.nus.edu.sg/handle/10635/181397
ISSN: 14712180
DOI: 10.1186/s12866-016-0624-8
Rights: Attribution 4.0 International
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