ArticleVirulence2018
Both live and dead Enterococci activate Caenorhabditis elegans host defense via immune and stress pathways.
Article in Virulence, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed.
- Worming out defence strategies: mechanisms of immunity through the lens of genetic screens in C. elegans.Heredity · 2026Review
- A gut-activated NHR-86-CYP pathway mediates the neuroprotective effects of Enterococcus faecium probiotics in a nematode model of amyotrophic lateral sclerosis.PLoS biology · 2026Article
- Pathogenicity and intestinal barrier disruptive ability ofFEMS microbes · 2026Article
- Bacterial exopolysaccharides mediate activation of flavin-containing monooxygenase 2 to extend lifespan in Caenorhabditis elegans.Cell communication and signaling : CCS · 2025Article
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- Perception ofmicroPublication biology · 2025Article
- A diet of oxidative stress-adapted bacteria improves stress resistance and lifespan inScience advances · 2024Article
- ADARs regulate cuticle collagen expression and promote survival to pathogen infection.BMC biology · 2024Article
- An organismal understanding of C. elegans innate immune responses, from pathogen recognition to multigenerational resistance.Seminars in cell & developmental biology · 2024Review
- Polyethylene glycol as an improved barrier to prevent fleeing inmicroPublication biology · 2024Article
- Lysosome-related organelles promote stress and immune responses in C. elegans.Communications biology · 2023Article
- Ancestral glycoprotein hormone-receptor pathway controls growth inFrontiers in endocrinology · 2023Article
- Small RNAs couple embryonic developmental programs to gut microbes.Science advances · 2022Article
- Wild-type Caenorhabditis elegans isolates exhibit distinct gene expression profiles in response to microbial infection.BMC genomics · 2022Article
- The transcription factor HLH-26 controls probiotic-mediated protection against intestinal infection through up-regulation of the Wnt/BAR-1 pathway.PLoS biology · 2022Article
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- Article
- Host Preference of Beneficial Commensals in a Microbially-Diverse Environment.Frontiers in cellular and infection microbiology · 2022Article
- Article
- Nuclear hormone receptors promote gut and glia detoxifying enzyme induction and protect C. elegans from the mold P. brevicompactum.Cell reports · 2021Article
Corrections and comments
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2 authors.
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Abstract
The innate immune response of the nematode Caenorhabditis elegans has been extensively studied and a variety of Toll-independent immune response pathways have been identified. Surprisingly little, however, is known about how pathogens activate the C. elegans immune response. Enterococcus faecalis and Enterococcus faecium are closely related enterococcal species that exhibit significantly different levels of virulence in C. elegans infection models. Previous work has shown that activation of the C. elegans immune response by Pseudomonas aeruginosa involves P. aeruginosa-mediated host damage. Through ultrastructural imaging, we report that infection with either E. faecalis or E. faecium causes the worm intestine to become distended with proliferating bacteria in the absence of extensive morphological changes and apparent physical damage. Genetic analysis, whole-genome transcriptional profiling, and multiplexed gene expression analysis demonstrate that both enterococcal species, whether live or dead, induce a rapid and similar transcriptional defense response dependent upon previously described immune signaling pathways. The host response to E. faecium shows a stricter dependence upon stress response signaling pathways than the response to E. faecalis. Unexpectedly, we find that E. faecium is a C. elegans pathogen and that an active wild-type host defense response is required to keep an E. faecium infection at bay. These results provide new insights into the mechanisms underlying the C. elegans immune response to pathogen infection.
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