ArticleVirulence2017
Role of GATA transcription factor ELT-2 and p38 MAPK PMK-1 in recovery from acute P. aeruginosa infection in C. elegans.
Article in Virulence, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 61 citations in OpenAlex.
- Neural regulation of infection resolution prevents ER stress and tissue damage.bioRxiv : the preprint server for biology · 2026Article
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- Serotonin deficiency from constitutive SKN-1 activation drives pathogen apathy.Nature communications · 2024Article
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- ADARs regulate cuticle collagen expression and promote survival to pathogen infection.BMC biology · 2024Article
- Neuronal NPR-15 modulates molecular and behavioral immune responses via the amphid sensory neuron-intestinal axis inbioRxiv : the preprint server for biology · 2024Article
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- Paeoniflorin increases the survival of Pseudomonas aeruginosa infected Caenorhabditis elegans at the immunosuppression stage by activating PMK-1, BAR-1, and EGL-1 signals.Archives of pharmacal research · 2023Article
- Treatment with paeoniflorin increases lifespan ofFrontiers in pharmacology · 2023Article
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- A Surface Exposed, Two-Domain Lipoprotein Cargo of a Type XI Secretion System Promotes Colonization of Host Intestinal Epithelia Expressing Glycans.Frontiers in microbiology · 2022Article
- Beneficial effect of Xuebijing againstFrontiers in pharmacology · 2022Article
- Immunity-longevity tradeoff neurally controlled by GABAergic transcription factor PITX1/UNC-30.Cell reports · 2021Article
- Take a Walk to the Wild Side ofMicrobiology and molecular biology reviews : MMBR · 2021Review
- Loss of Function of Scavenger Receptor SCAV-5 ProtectsFrontiers in cellular and infection microbiology · 2021Article
- Innate immunity in C. elegans.Current topics in developmental biology · 2021Review
- The C. elegans GATA transcription factor elt-2 mediates distinct transcriptional responses and opposite infection outcomes towards different Bacillus thuringiensis strains.PLoS pathogens · 2020Article
- G-Protein-Coupled Receptor SRBC-48 Protects against Dendrite Degeneration and Reduced Longevity Due to Infection.Cell reports · 2020Article
- Article
- Redirection of SKN-1 abates the negative metabolic outcomes of a perceived pathogen infection.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
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3 authors at 2 institutions in 1 country.
Funding
Abstract
Infectious diseases caused by bacterial pathogens reduce the fitness of their associated host but are generally limited in duration. In order for the diseased host to regain any lost fitness upon recovery, a variety of molecular, cellular, and physiological processes must be employed. To better understand mechanisms underlying the recovery process, we have modeled an acute Pseudomonas aeruginosa infection in C. elegans using brief exposures to this pathogen and subsequent antibiotic treatment. To identify host genes altered during recovery from P. aeruginosa infection, we performed whole genome expression profiling. The analysis of this dataset indicated that the activity of the host immune system is down-regulated upon recovery and revealed shared and pathogen-specific host responses during recovery. We determined that the GATA transcription factor ELT-2 and the p38 MAP kinase PMK-1 are necessary for animals to successfully recover from an acute P. aeruginosa infection. In addition, we found that ELT-2 plays a more prominent and earlier role than PMK-1 during recovery. Our data sheds further light on the molecular mechanisms and transcriptional programs involved in recovery from an acute bacterial infection, which provides a better understanding of the entire infectious disease process.
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Registered trials
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.