Gpr37 modulates the severity of inflammation-induced GI dysmotility by regulating enteric reactive gliosis

The enteric nervous system (ENS) is contained within two layers of the gut wall and is made up of neurons, immune cells, and enteric glia cells (EGCs) that regulate gastrointestinal (GI) function. EGCs in both inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) change in response to...

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Published inbioRxiv : the preprint server for biology
Main Authors Robertson, Keiramarie, Hahn, Oliver, Robinson, Beatriz G, Faruk, Arwa T, Janakiraman, Mathangi, Namkoong, Hong, Kim, Kwangkon, Ye, Jiayu, Bishop, Estelle Spear, Hall, Randy A, Wyss-Coray, Tony, Becker, Laren S, Kaltschmidt, Julia A
Format Journal Article
LanguageEnglish
Published United States 12.04.2024
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Summary:The enteric nervous system (ENS) is contained within two layers of the gut wall and is made up of neurons, immune cells, and enteric glia cells (EGCs) that regulate gastrointestinal (GI) function. EGCs in both inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) change in response to inflammation, referred to as reactive gliosis. Whether EGCs restricted to a specific layer or region within the GI tract alone can influence intestinal immune response is unknown. Using bulk RNA-sequencing and hybridization, we identify G-protein coupled receptor , as a gene expressed only in EGCs of the myenteric plexus, one of the two layers of the ENS. We show that Gpr37 contributes to key components of LPS-induced reactive gliosis including activation of NF-kB and IFN-y signaling and response genes, lymphocyte recruitment, and inflammation-induced GI dysmotility. Targeting Gpr37 in EGCs presents a potential avenue for modifying inflammatory processes in the ENS.