ArticleBMC microbiology2016
Caenorhabditis elegans susceptibility to gut Enterococcus faecalis infection is associated with fat metabolism and epithelial junction integrity.
Article in BMC microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
27 citing papers in PubMed, 51 citations in OpenAlex.
- The GPCR NMUR-1 mediates neural regulation of energy homeostasis in response to pathogen infection.Infection and immunity · 2025Article
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- Screening of Microorganisms Isolated from Stingless Bees' Larval Food in the Biocontrol ofJournal of nematology · 2025Article
- Geroprotective Effect of Levilactobacillus brevis and Weizmannia coagulans in Caenorhabditis elegans.Probiotics and antimicrobial proteins · 2024Article
- Effects of feces storage conditions for host-microbiota screenings inFrontiers in microbiomes · 2024Article
- Transcriptional suppression of sphingolipid catabolism controls pathogen resistance in C. elegans.PLoS pathogens · 2023Article
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- Caenorhabditis elegans for research on cancer hallmarks.Disease models & mechanisms · 2023Article
- Juxtaposing Caenorhabditis elegans-Pathogenic Mould Model with Other Models; How Reliable Is This Nematode Model? A Mini Review.Current microbiology · 2023Review
- Application ofInternational journal of molecular sciences · 2023Review
- Impaired immune response and barrier function in GSPD-1-deficientCurrent research in microbial sciences · 2023Article
- Article
- Nuclear hormone receptor NHR-49 is an essential regulator of stress resilience and healthy aging inFrontiers in physiology · 2023Review
- A gonadal gap junction INX-14/Notch GLP-1 signaling axis suppresses gut defense through an intestinal lysosome pathway.Frontiers in immunology · 2023Article
- Wild-type Caenorhabditis elegans isolates exhibit distinct gene expression profiles in response to microbial infection.BMC genomics · 2022Article
- NHR-49/PPAR-α and HLH-30/TFEB cooperate foreLife · 2021Article
- Novel Immune Modulators EnhancemSphere · 2021Article
- Immunometabolism in Caenorhabditis elegans.PLoS pathogens · 2020Article
- NHR-49 Transcription Factor Regulates Immunometabolic Response and Survival of Caenorhabditis elegans during Enterococcus faecalis Infection.Infection and immunity · 2020Article
- IGLR-2, a Leucine-Rich Repeat Domain Containing Protein, Is Required for the Host Defense inFrontiers in immunology · 2020Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGut 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.
resultsAn 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.
conclusionsThe 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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.