Mouse gut metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1006727 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Composition of colonic microbes in mice deficient in intestinal Treg subsets
| PRJNA1010695 | ENA
Project description:Regulatory T cells (Tregs) are immune cells that play a crucial role in maintaining tolerance to harmless antigens, including commensal microbes. In the intestine, Tregs can be classified into subsets based on their expression of transcription factors Helios, Rorg, Gata3 and cMaf. The exact functions of the intestinal Treg subsets and their role in maintaining tolerance to intestinal microbes is not fully understood. Here, we generated conditional knockout mice of each Treg subset and profiled the composition of their intestinal microbiota by performing 16S rRNA sequencing of stool from conditional knockouts and matched littermate controls.
2023-12-20 | GSE241887 | GEO
Project description:Foxp3+ regulatory T cells (Tregs) in the colon are key to promoting peaceful co-existence with symbiotic microbes. Differentiated in either thymic or peripheral locations, and modulated by microbes and other cellular influencers, colonic Treg subsets have been identified through key transcription factors (TF; Helios, Rorg, Gata3, cMaf), but their inter-relationships are unclear. Here, we perform genomic analysis of colonic lamina propria Tregs with conditional KOs of each of these TFs to better understand how each TF contributes to colonic Treg identity and function.
2023-12-20 | GSE240657 | GEO
Project description:Host-pathogen interactions involve two critical strategies: resistance, whereby hosts clear invading microbes, and tolerance, whereby hosts carry high pathogen burden asymptomatically. Here, we investigate mechanisms by which Salmonella- superspreader hosts (SSP) maintain an asymptomatic state during chronic infection. We found that regulatory T cells (Tregs) are essential for this disease-tolerant state, limiting intestinal immunopathology and enabling SSP hosts to thrive, while facilitating Salmonella transmission. Treg depletion in SSP mice resulted in decreased survival, heightened gut inflammation and impairment of the intestinal barrier, without affecting Salmonella persistence. Colonic Tregs from SSP mice exhibited a unique transcriptomic profile characterized by the upregulation type-1 inflammatory genes, including the transcription factor T-bet. In the absence of Tregs, we observed robust expansion of cytotoxic CD4+ T cells, with CD4+ T cell depletion restoring homeostasis. These results uncover a critical host strategy to establish disease tolerance during chronic enteric infection, providing novel insights into mucosal responses to persistent pathogens and chronic intestinal inflammation.
2025-08-19 | GSE303864 | GEO
Project description:Host-pathogen interactions involve two critical strategies: resistance, whereby hosts clear invading microbes, and tolerance, whereby hosts carry high pathogen burden asymptomatically. Here, we investigate mechanisms by which Salmonella- superspreader hosts (SSP) maintain an asymptomatic state during chronic infection. We found that regulatory T cells (Tregs) are essential for this disease-tolerant state, limiting intestinal immunopathology and enabling SSP hosts to thrive, while facilitating Salmonella transmission. Treg depletion in SSP mice resulted in decreased survival, heightened gut inflammation and impairment of the intestinal barrier, without affecting Salmonella persistence. Colonic Tregs from SSP mice exhibited a unique transcriptomic profile characterized by the upregulation type-1 inflammatory genes, including the transcription factor T-bet. In the absence of Tregs, we observed robust expansion of cytotoxic CD4+ T cells, with CD4+ T cell depletion restoring homeostasis. These results uncover a critical host strategy to establish disease tolerance during chronic enteric infection, providing novel insights into mucosal responses to persistent pathogens and chronic intestinal inflammation.
2025-08-19 | GSE302695 | GEO
Project description:While fermentable oligo- and di-, mono-saccharides and polyols (FODMAPs) have been implicated in exacerbating inflammatory bowel disease (IBD) symptoms, the exact influence of FODMAPs on gut microbiota and inflammation is unclear. Here, we show that sorbitol, a polyol, exacerbates colitis in mice induced by dextran sodium sulfate (DSS). Sorbitol increases the expression of inflammatory genes including Il1b in the colon, associated with M1 macrophage-related genes elevated in IBD patients. Indeed, sorbitol treatment leads to a higher proportion of M1 macrophages in the colon, worsening colitis, which is reversed in IL-1β-deficient mice and mitigated with antibiotic treatment. Sorbitol alters the composition of gut microbiota and metabolites, with Prevotellaceae and tryptamine positively correlated with colonic M1 macrophages. Tryptamine stimulation enhances M1 macrophage polarization. Taken together, polyol consumption activates intestinal macrophages by altering the gut microbiome, which in turn promotes intestinal inflammation.
2025-06-14 | GSE299433 | GEO
Project description:Instability in the composition of gut bacterial communities, referred as dysbiosis, has been associated with important human intestinal disorders such as Crohn’s disease and colorectal cancer. Our data showed that Nod2-mediated risk of intestinal inflammation in colitis model is communicable to WT mice by cohousing. Here, we investigated if Nod2-deficient mice microbiota is able to change transcript profiles in Nod2-immunocompetent mice (C57Bl6/J mice) independently of colitis. Analysis used RNA extracted from colonic mucosa of C57Bl/6J mice co-housed with Nod2-deficient mice and C57Bl/6J mice alone. Direct comparisons of 4 biologicals replicates of C57Bl/6J mice cohoused with Nod2-deficient mice vs C57Bl/6J mice were performed.
2013-01-02 | E-GEOD-36481 | biostudies-arrayexpress
Project description:Instability in the composition of gut bacterial communities, referred as dysbiosis, has been associated with important human intestinal disorders such as CrohnM-bM-^@M-^Ys disease and colorectal cancer. Here, we show that dysbiosis coupled to Nod2 or Rip2 deficiency suffices to cause an increased risk for intestinal inflammation and colitis-associated carcinogenesis in mice. Aggravated epithelial lesions and dysplasia upon chemical-induced injury associated with loss of Nod2 or Rip2 can be prevented by antibiotics or anti-IL6R treatment. Nod2-mediated risk for intestinal inflammation and colitis-associated tumorigenesis is communicable through maternally-transmitted microbiota even to wild-type hosts. Disease progression was identified to drive complex NOD2-dependent changes of the colonic-associated microbiota. Reciprocal microbiota transplantation rescues the vulnerability of Nod2-deficient mice to colonic injury. Altogether, our results unveil an unexpected function for NOD2 in shaping a protective assembly of gut microbial communities, providing a rationale for intentional manipulation of genotype-dependent dysbiosis as a causative therapeutic principle in chronic intestinal inflammation. Analysis used RNA extracted from colonic mucosa of untreated, antibiotics-treated or metronidazole-treated C57Bl/6J and Nod2-deficient mice in CAC model. Direct comparisons were performed as follow: C57Bl/6J untreated mice vs Nod2-deficient untreated mice, C57Bl/6J antibiotics-treated mice vs Nod2-deficient antibiotics-treated mice, C57Bl/6J metronidazole-treated mice vs Nod2-deficient metronidazole-treated mice, C57Bl/6J untreated mice vs C57Bl/6J antibiotics-treated mice, C57Bl/6J untreated mice vs C57Bl/6J metronidazole-treated mice, Nod2-deficient untreated mice vs Nod2-deficient antibiotics-treated mice, Nod2-deficient untreated mice vs Nod2-deficient metronidazole-treated mice. Indirect comparisons with control data were made across multiple arrays with raw data pulled from different channels for data analysis.
2013-01-02 | E-GEOD-32421 | biostudies-arrayexpress
Project description:Multiple sclerosis (MS) is a chronic inflammatory, demyelinating disease of the central nervous system. The pathogenesis of MS and other autoimmune diseases is defined by a disrupted equilibrium between IL-17A-producing CD4 T cells (Th17) and regulatory CD4 T cells (Treg). The development of Treg and Th17 cells can be regulated by the gut microbiota, however, it is unclear how the gut microbiota is impacted by IL-17A and how this, in turn, modulates Treg and disease. Here, we show that IL-17A deficiency promotes interferon-I-related gene expression and expands gut microbes that induce the Treg cells, resulting in milder disease in a mouse model of MS. Utilizing HLA-DR3.IL17A-/- transgenic mice, we showed significant enrichment of Treg-promoting gut microbes such as Prevotella sp. MGM1, Parabacteroides distasonis and Bacteroides sartorii species. Further, we observed enrichment of bacterial-specific short-chain fatty acid metabolic pathways that promote Treg function in HLA-DR3.IL17A-/- transgenic mice. Notably, disease severity was reversed in IL-17A sufficient mice that received fecal transplants from, and cohoused with, IL-17A-deficient mice, highlighting a critical role for the gut microbiota in inducing Treg and reducing disease severity. Collectively, we show that IL-17A is an important regulator of the gut microbiota-Treg axis, which mediates immune homeostasis, inflammation, and diseases such as MS.
2025-10-01 | GSE190048 | GEO
Project description:The colonic lamina propria contains a distinct population of Foxp3+ T regulatory cells (Tregs) that modulate responses to commensal microbes. Analysis of gene expression revealed that the transcriptome of colonic Tregs is distinct from splenic and other tissue Tregs. Rorγ and Helios in colonic Tregs mark distinct populations: Rorγ+Helios- or Rorγ-Helios+ Tregs. We uncovered an unanticipated role for Rorγ, a transcription factor generally considered to be antagonistic to Foxp3. Rorγ in colonic Tregs accounts for a small but specific part of the colon-specific Treg signature. (1) Total colonic and splenic Foxp3+ Treg comparison: Lymphocytes were isolated from colonic lamina propria and spleens of Foxp3-ires-GFP mice, where GFP reports Foxp3 expression. TCRb+CD4+GFP+ cells were double sorted into Trizol. (2) Colonic Rorγ+ and Rorγ- Treg comparison: Foxp3-ires-Thy1.1 reporter mice were crossed to Rorc-GFP reporter mice to generate mice that report both Foxp3 and Rorγ expression. Rorγ+Foxp3+ Tregs (TCRb+CD4+Thy1.1+GFP+) and Rorγ-Foxp3+ Tregs (TCRb+CD4+Thy1.1+GFP-) from colonic lamina propria were double sorted into Trizol.To reduce variability and increase cell number, cells from multiple mice were pooled for sorting and at least three replicates were generated for all groups. RNA from 1.5-3.0 x104 cells was amplified, labeled and hybridized to Affymetrix Mouse Gene 1.0 ST Arrays.
2015-07-25 | E-GEOD-68009 | biostudies-arrayexpress