Enteric glia regulate Paneth cell secretion and intestinal microbial ecology
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ABSTRACT:
PROVIDER: PRJNA1178611 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31141856_1.fastq.gz | Fastqsanger.gz | |||
| SRR31141856_2.fastq.gz | Fastqsanger.gz | |||
| SRR31141857_1.fastq.gz | Fastqsanger.gz | |||
| SRR31141857_2.fastq.gz | Fastqsanger.gz | |||
| SRR31141858_1.fastq.gz | Fastqsanger.gz |
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Project description:Glial cells of the enteric nervous system (ENS) interact closely with the intestinal epithelium and secrete signals that influence epithelial cell proliferation and barrier formation in vitro. Whether these interactions are important in vivo, however, is unclear because previous studies reached conflicting conclusions. To better define the roles of enteric glia in steady state regulation of the intestinal epithelium, we characterized the glia in closest proximity to epithelial cells and found that the majority express PLP1 in both mice and humans. To test their functions using an unbiased approach, we genetically depleted PLP1+ cells in mice and transcriptionally profiled the small and large intestines. Surprisingly, glial loss had minimal effects on transcriptional programs and the few identified changes varied along the gastrointestinal tract. In the ileum, where enteric glia had been considered most essential for epithelial integrity, glial depletion did not drastically alter epithelial gene expression but caused a modest enrichment in signatures of Paneth cells, a secretory cell type important for innate immunity. In the absence of PLP1+ glia, Paneth cell number was intact, but a subset appeared abnormal with irregular and heterogenous cytoplasmic granules, suggesting a secretory deficit. Consistent with this possibility, ileal explants from glial-depleted mice secreted less functional lysozyme than controls with corresponding effects on fecal microbial composition. Collectively, these data suggest that enteric glia do not exert broad effects on the intestinal epithelium but have an essential role in regulating Paneth cell function and gut microbial ecology.
2024-12-01 | GSE280442 | GEO
Project description: Not available
| S-EPMC11996175 | biostudies-literature
Project description:To identify the gene expression profile of enteric glia and assess the transcriptional similarity between enteric and extraenteric glia, we performed RNA sequencing analysis on PLP1-expressing cells in the mouse intestine. This analysis shows that enteric glia are transcriptionally unique and distinct from other cell types in the nervous system. Enteric glia express many genes characteristic of the myelinating glia, Schwann cells and oli- godendrocytes, although there is no evidence of myelination in the murine ENS. Total RNA expression profiles of PLP1 expressing enteric glial cells (GFP+) and non-glial cells (GFP-negative) were obtained from the ileum and colon of juvenile PLP1-eGFP transgenic mice.
2015-09-01 | E-GEOD-72560 | biostudies-arrayexpress
Project description:BACKGROUND Enteric glia contribute to the pathophysiology of various intestinal immune-driven diseases, such as postoperative ileus (POI), a motility disorder and common complication after abdominal surgery. Enteric gliosis of the intestinal muscularis externa (ME) has been identified as part of POI development. However, the glia-restricted responses and activation mechanisms are poorly understood. The sympathetic nervous system becomes rapidly activated by abdominal surgery. It modulates intestinal immunity, innervates all intestinal layers, and directly interfaces with enteric glia. We hypothesized that sympathetic innervation controls enteric glia reactivity in response to surgical trauma. METHODS Sox10iCreERT2/Rpl22HA/+ mice were subjected to a mouse model of laparotomy or intestinal manipulation to induce POI. Histological, protein, and transcriptomic analyses were performed to analyze glia-specific responses. Interactions between the sympathetic nervous system and enteric glia were studied in mice chemically depleted of TH+ sympathetic neurons and glial-restricted Sox10iCreERT2/JellyOPfl/+/Rpl22HA/+ mice, allowing optogenetic stimulation of β-adrenergic downstream signaling and glial-specific transcriptome analyses. A laparotomy model was used to study the effect of sympathetic signaling on enteric glia in the absence of intestinal manipulation. Mechanistic studies included adrenergic receptor expression profiling in vivo and in vitro and adrenergic agonism treatments of primary enteric glial cell cultures to elucidate the role of sympathetic signaling in acute enteric gliosis and POI. RESULTS With ~4000 differentially expressed genes, the most substantial enteric glia response occurs early after intestinal manipulation. During POI, enteric glia switch into a reactive state and continuously shape their microenvironment by releasing inflammatory and migratory factors. Sympathetic denervation reduced the inflammatory response of enteric glia in the early postoperative phase. Optogenetic and pharmacological stimulation of β-adrenergic downstream signaling triggered enteric glia reactivity. Finally, distinct adrenergic agonists revealed β-1/2 adrenoceptors as the molecular targets of sympathetic–driven enteric glial reactivity. CONCLUSIONS Enteric glia act as early responders during post-traumatic intestinal injury and inflammation. Intact sympathetic innervation and active β-adrenergic receptor signaling in enteric glia is a trigger of the immediate glial postoperative inflammatory response. With immune-activating cues originating from the sympathetic nervous system as early as the initial surgical incision, adrenergic signaling in enteric glia presents a promising target for preventing POI development.
2023-11-15 | GSE198889 | GEO
Project description:The Experiment was performed to understand the changes in expression profile of enteric glia cells in context of intestinal inflammation. Enteric glia are crucial regulators of gastrointestinal motility, however enteric glia alterations in IBD are poorly characterized. Acute T-cell activation rapidly impacts enteric glia activation, and induces cell death pathways, which negatively impacts small intestinal transit. This experiment has been crucial to identify IFNγ- and TNFα -driven necrosis in activated glia cell subsets. In order to sequence pure enteric glia, a mouse strain of Bl6 mice with a Plp1CreERT insert for glial specificity crossed with mice with a flox controlled tdTomato fluorescent protein on the ROSA26 Locus. The mice received a peritoneal injection of an anti-CD3 antibody or its isotype control antibody. At 6 hours, the small intestine was collected and the longitudinal muscle layer with the myenteric plexus stripped off. After enzymatic dissociation and trituration, the enteric glia were FACS sorted and finally the RNA isolated.
2025-07-01 | E-MTAB-14876 | biostudies-arrayexpress
Project description:The Experiment was performed to understand the changes in expression profile of enteric glia cells in vitro to specific cytokines. Enteric glia are crucial regulators of gastrointestinal motility and immunity; however, it is not fully understood what specific cytokines can elicit a response in enteric glia. Acute T-cell activation rapidly impacts enteric glia activation, and induces cell death pathways, which negatively impacts small intestinal transit. Therefore, this experiment has been crucial to identify the specific responses of enteric glia to recombinant murine IFNγ, TNFα, Il-13, Il-17A and Il-1b. In order to sequence pure enteric glia, a mouse strain of Bl6 mice with a Plp1CreERT insert for glial specificity crossed with mice with a flox controlled tdTomato fluorescent protein on the ROSA26 Locus. From these mice the longitudinal muscle layer with the myenteric plexus stripped off and enzymaticly dissociated. The enteric glia were kept as a primary cell culture and the expression of tdTomato induced with 500 nM (Z)-4-Hydroxytamoxifen (MilliporeSigma). After expansion the glia were FACS sorted and stimulated with the respective cytokine. Finally, the RNA was isolated after 24 hours and sequenced.
2025-07-01 | E-MTAB-14879 | biostudies-arrayexpress
Project description:To identify the gene expression profile of enteric glia and assess the transcriptional similarity between enteric and extraenteric glia, we performed RNA sequencing analysis on PLP1-expressing cells in the mouse intestine. This analysis shows that enteric glia are transcriptionally unique and distinct from other cell types in the nervous system. Enteric glia express many genes characteristic of the myelinating glia, Schwann cells and oli- godendrocytes, although there is no evidence of myelination in the murine ENS.
2015-09-01 | GSE72560 | GEO
Project description:One of the largest populations of glia outside the brain is in the gut. These enteric glia are involved in many functions from intestinal peristalsis to immunity, yet it is unclear if there are defined types with distinct roles in homeostasis. Comparing glia from divergent microenvironments in the mouse intestine, we found that mucosal glia resembled microglia and macrophages, while muscularis glia resembled satellite glia. Tacr3, encoding the receptor for neuropeptide Neurokinin B (NKB), was enriched within muscularis glia associated with neuronal soma and was undetectable in extraintestinal glia. Genetic or pharmacological manipulation of NKB-TACR3 signaling disrupted establishment of enteric glial populations during postnatal development, and dynamically modulated intestinal motor behaviors in adult mice. Collectively, we delineate spatially, transcriptionally and functionally distinct populations of enteric glia, identify one as an unanticipated target of TACR3 antagonists in clinical use, and establish this pathway as necessary for enteric glial diversification and function.
2026-01-28 | GSE275795 | GEO
Project description:One of the largest populations of glia outside the brain is in the gut. These enteric glia are involved in many functions from intestinal peristalsis to immunity, yet it is unclear if there are defined types with distinct roles in homeostasis. Comparing glia from divergent microenvironments in the mouse intestine, we found that mucosal glia resembled microglia and macrophages, while muscularis glia resembled satellite glia. Tacr3, encoding the receptor for neuropeptide Neurokinin B (NKB), was enriched within muscularis glia associated with neuronal soma and was undetectable in extraintestinal glia. Genetic or pharmacological manipulation of NKB-TACR3 signaling disrupted establishment of enteric glial populations during postnatal development, and dynamically modulated intestinal motor behaviors in adult mice. Collectively, we delineate spatially, transcriptionally and functionally distinct populations of enteric glia, identify one as an unanticipated target of TACR3 antagonists in clinical use, and establish this pathway as necessary for enteric glial diversification and function.
2026-01-28 | GSE275794 | GEO