Ontology highlight
ABSTRACT:
PROVIDER: PRJNA743797 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15060654_1.fastq.gz | Fastqsanger.gz | |||
| SRR15060654_2.fastq.gz | Fastqsanger.gz | |||
| SRR15060655_1.fastq.gz | Fastqsanger.gz | |||
| SRR15060655_2.fastq.gz | Fastqsanger.gz | |||
| SRR15060656_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 40 |
Similar Datasets
Project description:Modulation of inflammation and parasite infection by cinnamaldehyde
| PRJNA694182 | ENA
Project description:Functional gastrointestinal (GI) tract disorders affect a substantial proportion of the global population and are often preceded by intestinal infections that cause injury to enteric neurons and glia through unrestrained immune responses. However, the mechanisms that limit infection-induced inflammation and protect the enteric nervous system remain poorly understood. Here, we investigated neuron-glia-macrophage interactions after West Nile virus (WNV) infection, a model neurotropic virus that causes GI tract dysmotility via injury of enteric neurons through a T cell-mediated cytolytic mechanism. In response to WNV infection, resident muscularis macrophages upregulate antiviral, proinflammatory, and immunomodulatory genes. However, pharmacological depletion of resident macrophages did not affect viral burden in the GI tract, but rather reshaped the enteric glial response to WNV, resulting in excessive production of T cell and neutrophil chemoattractants. This amplified recruitment of immune cells worsened enteric neuronal injury. Together, our findings identify resident muscularis macrophages as key regulators of glia-driven inflammation during enteric viral infection and reveal their role in protecting enteric neurons from immune-mediated damage.
2026-02-19 | GSE315460 | GEO
Project description:Functional gastrointestinal (GI) tract disorders affect a substantial proportion of the global population and are often preceded by intestinal infections that cause injury to enteric neurons and glia through unrestrained immune responses. However, the mechanisms that limit infection-induced inflammation and protect the enteric nervous system remain poorly understood. Here, we investigated neuron-glia-macrophage interactions after West Nile virus (WNV) infection, a model neurotropic virus that causes GI tract dysmotility via injury of enteric neurons through a T cell-mediated cytolytic mechanism. In response to WNV infection, resident muscularis macrophages upregulate antiviral, proinflammatory, and immunomodulatory genes. However, pharmacological depletion of resident macrophages did not affect viral burden in the GI tract, but rather reshaped the enteric glial response to WNV, resulting in excessive production of T cell and neutrophil chemoattractants. This amplified recruitment of immune cells worsened enteric neuronal injury. Together, our findings identify resident muscularis macrophages as key regulators of glia-driven inflammation during enteric viral infection and reveal their role in protecting enteric neurons from immune-mediated damage.
2026-02-19 | GSE315459 | GEO
Project description:Functional gastrointestinal (GI) tract disorders affect a substantial proportion of the global population and are often preceded by intestinal infections that cause injury to enteric neurons and glia through unrestrained immune responses. However, the mechanisms that limit infection-induced inflammation and protect the enteric nervous system remain poorly understood. Here, we investigated neuron-glia-macrophage interactions after West Nile virus (WNV) infection, a model neurotropic virus that causes GI tract dysmotility via injury of enteric neurons through a T cell-mediated cytolytic mechanism. In response to WNV infection, resident muscularis macrophages upregulate antiviral, proinflammatory, and immunomodulatory genes. However, pharmacological depletion of resident macrophages did not affect viral burden in the GI tract, but rather reshaped the enteric glial response to WNV, resulting in excessive production of T cell and neutrophil chemoattractants. This amplified recruitment of immune cells worsened enteric neuronal injury. Together, our findings identify resident muscularis macrophages as key regulators of glia-driven inflammation during enteric viral infection and reveal their role in protecting enteric neurons from immune-mediated damage.
2026-02-19 | GSE315457 | GEO
Project description:Functional gastrointestinal (GI) tract disorders affect a substantial proportion of the global population and are often preceded by intestinal infections that cause injury to enteric neurons and glia through unrestrained immune responses. However, the mechanisms that limit infection-induced inflammation and protect the enteric nervous system remain poorly understood. Here, we investigated neuron-glia-macrophage interactions after West Nile virus (WNV) infection, a model neurotropic virus that causes GI tract dysmotility via injury of enteric neurons through a T cell-mediated cytolytic mechanism. In response to WNV infection, resident muscularis macrophages upregulate antiviral, proinflammatory, and immunomodulatory genes. However, pharmacological depletion of resident macrophages did not affect viral burden in the GI tract, but rather reshaped the enteric glial response to WNV, resulting in excessive production of T cell and neutrophil chemoattractants. This amplified recruitment of immune cells worsened enteric neuronal injury. Together, our findings identify resident muscularis macrophages as key regulators of glia-driven inflammation during enteric viral infection and reveal their role in protecting enteric neurons from immune-mediated damage.
2026-02-19 | GSE315454 | GEO
Project description:Enteric neurons are essential regulators of intestinal physiology, yet their responses to varying microbial and immune environments along the intestinal tract and or during challenges remain poorly understood. Here, we regionally profile enteric neurons across gnotobiotic, allergic and parasite-infected mice. We demonstrate that timing and complexity of microbial perturbations and type 2 inflammation result in motor neuron state shifts and alter multiple functionally distinct sensory neurons, including IL-13- and leukotriene-responsive Nmu-hi cells and Grp-hi neurons, which expand in germ-free colonic tissue and interact with Grpr+ interstitial cells of Cajal. Leveraging AAV-based Perturb-seq to define genetic controllers of inhibitory motor neuron state transition, we identified Edf1 and Mitf as controllers of this program and of gastrointestinal transit time, directly linking enteric neuron states to physiology.
2025-10-30 | GSE301963 | GEO
Project description:Enteric neurons are essential regulators of intestinal physiology, yet their responses to varying microbial and immune environments along the intestinal tract and or during challenges remain poorly understood. Here, we regionally profile enteric neurons across gnotobiotic, allergic and parasite-infected mice. We demonstrate that timing and complexity of microbial perturbations and type 2 inflammation result in motor neuron state shifts and alter multiple functionally distinct sensory neurons, including IL-13- and leukotriene-responsive Nmu-hi cells and Grp-hi neurons, which expand in germ-free colonic tissue and interact with Grpr+ interstitial cells of Cajal. Leveraging AAV-based Perturb-seq to define genetic controllers of inhibitory motor neuron state transition, we identified Edf1 and Mitf as controllers of this program and of gastrointestinal transit time, directly linking enteric neuron states to physiology.
2025-10-30 | GSE302208 | GEO
Project description:Enteric neurons are essential regulators of intestinal physiology, yet their responses to varying microbial and immune environments along the intestinal tract and or during challenges remain poorly understood. Here, we regionally profile enteric neurons across gnotobiotic, allergic and parasite-infected mice. We demonstrate that timing and complexity of microbial perturbations and type 2 inflammation result in motor neuron state shifts and alter multiple functionally distinct sensory neurons, including IL-13- and leukotriene-responsive Nmu-hi cells and Grp-hi neurons, which expand in germ-free colonic tissue and interact with Grpr+ interstitial cells of Cajal. Leveraging AAV-based Perturb-seq to define genetic controllers of inhibitory motor neuron state transition, we identified Edf1 and Mitf as controllers of this program and of gastrointestinal transit time, directly linking enteric neuron states to physiology.
2025-10-30 | GSE302051 | GEO
Project description:CARD14 is an intracellular NF-κB signaling mediator in the skin, and rare CARD14 variants have been associated with psoriasis and atopic dermatitis. CARD14 is also expressed in intestinal epithelial cells (IEC). However, its function in the intestine remains unknown. We demonstrate here that transgenic mice expressing the psoriasis associated gain-of-function human CARD14(E138A) mutant specifically in IEC, show mild intestinal inflammation, without epithelial damage. Moreover, CARD14(E138A)IEC mice show a drastic reduction in intestinal motility, often associated with rectal prolapse. Enteric neuronal survival and functionality is unaffected in CARD14(E138A)IEC mice. Transcriptome analysis of IEC from CARD14(E138A)IEC mice reveals decreased expression of antimicrobial peptides by Paneth cells, accompanied with microbial dysbiosis and increased susceptibility to enteric bacterial infection. Our findings suggest that gain-of-function CARD14 mutations may not only predispose patients to psoriasis, but also mild intestinal inflammation, reduced intestinal motility and increased sensitivity to intestinal infection. CARD14(E138A)IEC mice are a valuable tool for further investigation of IEC-intrinsic molecular processes involved in intestinal inflammation and motility disorders.
2025-09-17 | GSE302705 | GEO
Project description:Cinnamaldehyde and carvacrol modulated gene expression induced by parasite antigen in monocytes, with an upregulated of an antioxidant defense network
2025-12-08 | GSE312280 | GEO