ArticleScientific reports2016
Neuronal GPCR OCTR-1 regulates innate immunity by controlling protein synthesis in Caenorhabditis elegans.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- Neural regulation of infection resolution prevents ER stress and tissue damage.bioRxiv : the preprint server for biology · 2026Article
- NMDA Receptor Subunit NMR-2 Regulates Pathogen-Induced Immune Responses via the Nervous System inbioRxiv : the preprint server for biology · 2026Article
- Single-type neuron transcriptomics uncovers cell-type-specific regulators of host defense inbioRxiv : the preprint server for biology · 2026Article
- Intersections between proteostasis and immunity: insights from Caenorhabditis elegans.Disease models & mechanisms · 2026Review
- Neurotransmitter signaling in molecular and behavioral immune responses to pathogens inMicrobiology and molecular biology reviews : MMBR · 2025Review
- The GPCR NMUR-1 mediates neural regulation of energy homeostasis in response to pathogen infection.Infection and immunity · 2025Article
- The GCN-2/eIF-2α/ATF-4 signaling pathway is involved inVirulence · 2025Article
- TheiScience · 2025Article
- GPCR Sense Communication Among Interaction Nematodes with Other Organisms.International journal of molecular sciences · 2025Review
- The MAB-5/Hox family transcription factor is important for Caenorhabditis elegans innate immune response to Staphylococcus epidermidis infection.G3 (Bethesda, Md.) · 2024Article
- ThemBio · 2024Article
- AdvancingPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Review
- Using single-worm RNA sequencing to study C. elegans responses to pathogen infection.BMC genomics · 2022Article
- Glutamate signaling mediatesiScience · 2022Article
- Article
- Reduced CaFrontiers in neuroscience · 2022Article
- Detection of Pathogens and Regulation of Immunity by the Caenorhabditis elegans Nervous System.mBio · 2021Review
- Biological Age Prediction From Wearable Device Movement Data Identifies Nutritional and Pharmacological Interventions for Healthy Aging.Frontiers in aging · 2021Article
- Innate immunity in C. elegans.Current topics in developmental biology · 2021Review
- Neuro-immune communication inCurrent research in immunology · 2021Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Upon pathogen infection, microbial killing pathways and cellular stress pathways are rapidly activated by the host innate immune system. These pathways must be tightly regulated because insufficient or excessive immune responses have deleterious consequences. Increasing evidence indicates that the nervous system regulates the immune system to confer coordinated protection to the host. However, the precise mechanisms of neural-immune communication remain unclear. Previously we have demonstrated that OCTR-1, a neuronal G protein-coupled receptor, functions in the sensory neurons ASH and ASI to suppress innate immune responses in non-neural tissues against Pseudomonas aeruginosa in Caenorhabditis elegans. In the current study, by using a mass spectrometry-based quantitative proteomics approach, we discovered that OCTR-1 regulates innate immunity by suppressing translation and the unfolded protein response (UPR) pathways at the protein level. Functional assays revealed that OCTR-1 inhibits specific protein synthesis factors such as ribosomal protein RPS-1 and translation initiation factor EIF-3.J to reduce infection-triggered protein synthesis and UPR. Translational inhibition by chemicals abolishes the OCTR-1-controlled innate immune responses, indicating that activation of the OCTR-1 pathway is dependent on translation upregulation such as that induced by pathogen infection. Because OCTR-1 downregulates protein translation activities, the OCTR-1 pathway could function to suppress excessive responses to infection or to restore protein homeostasis after infection.
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