ArticleNeurogastroenterology and motility2023
Stimulator of interferon genes (STING) expression in the enteric nervous system and contributions of glial STING in disease.
Article in Neurogastroenterology and motility, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- The interaction of enteric glial cells and gut microbiota in health and diseases.Science China. Life sciences · 2026Article
- Article
- Mechanisms of enteric neuropathy in diverse contexts of gastrointestinal dysfunction.Neurogastroenterology and motility · 2025Review
- Inflammatory Bowel Disease (IBD)-Associated Colorectal Cancer (CRC): Is cGAS-STING Pathway Targeting the Key to Chemoprevention?International journal of molecular sciences · 2025Review
- The Physiology of Enteric Glia.Annual review of physiology · 2025Review
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAppropriate host-microbe interactions are essential for enteric glial development and subsequent gastrointestinal function, but the potential mechanisms of microbe-glial communication are unclear. Here, we tested the hypothesis that enteric glia express the pattern recognition receptor stimulator of interferon genes (STING) and communicate with the microbiome through this pathway to modulate gastrointestinal inflammation.
methodsIn situ transcriptional labeling and immunohistochemistry were used to examine STING and IFNβ expression in enteric neurons and glia. Glial-STING KO mice (Sox10
resultsEnteric glia and neurons express STING, but only enteric neurons express IFNβ. While both the myenteric and submucosal plexuses produce IFNβ with STING activation, enteric glial STING plays a minor role in its production and seems more involved in autophagy processes. Furthermore, deleting enteric glial STING does not affect weight loss, colitis severity, or neuronal cell proportions in the DSS colitis model.
conclusionTaken together, our data support canonical roles for STING and IFNβ signaling in the enteric nervous system through enteric neurons but that enteric glia do not use these same mechanisms. We propose that enteric glial STING may utilize alternative signaling mechanisms and/or is only active in particular disease conditions. Regardless, this study provides the first glimpse of STING signaling in the enteric nervous system and highlights a potential avenue of neuroglial-microbial communication.
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