Affiliation:
1. Department of Physiology, Neuroscience Program Michigan State University East Lansing Michigan USA
2. College of Human Medicine Michigan State University East Lansing Michigan USA
Abstract
AbstractBackgroundAppropriate 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 (Sox10CreERT2+/−;STINGfl/fl) and IFNβ ELISA were used to characterize the role of enteric glia in canonical STING activation. The role of glial STING in gastrointestinal inflammation was assessed in the 3% DSS colitis model.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.
Funder
National Institute of Diabetes and Digestive and Kidney Diseases
Subject
Gastroenterology,Endocrine and Autonomic Systems,Physiology
Cited by
1 articles.
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