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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 |
Appears in Collections: | Elements Staff Publications |
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