Mouse gut metagenome
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR198953_1.fastq.gz | Fastqsanger.gz | |||
| DRR198953_2.fastq.gz | Fastqsanger.gz | |||
| DRR198954_1.fastq.gz | Fastqsanger.gz | |||
| DRR198954_2.fastq.gz | Fastqsanger.gz | |||
| DRR198955_1.fastq.gz | Fastqsanger.gz |
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Project description:Inflammatory caspases are essential effectors of inflammation and cell death. Here, we investigated their roles in colitis and colorectal cancer and report a bimodal regulation of intestinal homeostasis, inflammation and tumorigenesis by caspases-1 and -12. Casp1-/- mice exhibited defects in mucosal tissue repair and succumbed rapidly after dextran sulfate sodium (DSS) administration. This phenotype was rescued by administration of exogenous interleukin-18 and was partially reproduced in mice deficient in the inflammasome adaptor ASC. Casp12-/- mice, in which the inflammasome is derepressed, were resistant to acute colitis and showed signs of enhanced repair. Together with their increased inflammatory response, the enhanced repair response of Casp12-/- mice rendered them more susceptible to colorectal cancer induced by azoxymethane (AOM)+DSS. Taken together, our results indicate that the inflammatory caspases are critical in the induction of inflammation in the gut following injury, which is necessary for tissue repair and maintenance of immune tolerance. Total RNA obtained from isolated tumors or normal colon tissue from wild type and caspase-12 deficient mice were compared.
2010-07-30 | E-GEOD-20407 | biostudies-arrayexpress
Project description:Intestinal microbial dysbiosis is associated with Crohn’s disease (CD). However, the mechanisms leading to the chronic mucosal inflammation that characterizes this disease remain unclear. To evaluate causality and mechanisms of disease, we conducted a systems level study of the interactions between the gut microbiota and host in new-onset pediatric patients. We report an altered host proteome in CD patients indicative of impaired mitochondrial functions. A downregulation of mitochondrial proteins implicated in H2S detoxification was observed, while the relative abundance of H2S microbial producers was increased. Network correlation analysis identified Atopobium parvulum as the central hub of H2S producers. Gnotobiotic and conventionalized colitis-susceptible interleukin-10-deficient (Il10-/-) mice demonstrated that A. parvulum induced colitis, a phenotype requiring the presence of the intestinal microbiota. Administration of bismuth, a H2S scavenger, prevented A. parvulum-induced colitis in Il10-/- mice. This study identified host-microbiota interactions that are disturbed in CD patients providing mechanistic insights on CD pathogenesis.
2016-09-29 | PXD002882 | Pride
Project description:Background; MUC2 mucin produced by intestinal goblet cells is the major component of the intestinal mucus barrier. MUC2 homo-oligomerizes intracellularly into large secreted polymers which give mucus its viscous properties. The inflammatory bowel disease (IBD) ulcerative colitis is characterized by depleted goblet cells and a reduced mucus layer, whereas goblet cells and the mucus layer are increased in the other major inflammatory bowel disease, Crohnâs disease. Methods and Findings; By murine N-ethyl-N-nitrosourea-mutagenesis we identified two distinct non-complementing missense mutations in Muc2 exons encoding N- and C-terminal homo-oligomerization domains causing an ulcerative colitis-like phenotype. Both strains developed mild spontaneous distal intestinal inflammation, chronic diarrhea, rectal bleeding and prolapse, increased susceptibility to acute and chronic colitis induced by a luminal toxin, aberrant Muc2 biosynthesis, smaller goblet cell thecae (less stored mucin) and a diminished mucus barrier. Enhanced local production of IL-1beta, TNF-alpha and IFN-gamma was seen in the distal colon. The number of leukocytes within mesenteric lymph nodes was increased five-fold and leukocytes cultured in vitro produced both Th1 and Th2 cytokines (IFN-gamma, TNF-alpha and IL-13). Intestinal permeability was increased and the luminal bacterial flora were more heavily coated with immunoglobulin as occurs in IBD. This pathology was accompanied by accumulation of the Muc2 precursor and ultrastructural and biochemical evidence of endoplasmic reticulum (ER) stress in goblet cells, activation of the unfolded protein response, and altered intestinal expression of genes involved in ER stress, inflammation, apoptosis and wound repair. Expression of mutated Muc2 oligomerization domains in vitro demonstrated that aberrant Muc2 oligomerization underlies the ER stress. These models show that mutations in Muc2 oligomerization domains can lead to aberrant assembly of the Muc2 complex leading to ER stress, a depleted mucus barrier and intestinal inflammation. In ulcerative colitis we demonstrate similar accumulation of non-glycosylated MUC2 precursor in goblet cells together with ultrastructural and biochemical evidence of ER stress even in non-inflamed intestinal tissue. Conclusions; The observations that mucin misfolding and ER stress lead directly to intestinal inflammation and that ER stress and goblet cell pathology occur in ulcerative colitis suggest that ER stress-related mucin depletion could be a fundamental component of the pathogenesis of colitis. Experiment Overall Design: 3 individual mice from the Eeyore, Winnie or Wild-type strains were compared as groups. An Affymetrix ID was compared between groups if the ID was Present within two of the three mice within each grouping. IDs were compared by calculating the log2 of Group One average signal divided by Group 2 average signal.
2008-04-06 | E-GEOD-9913 | biostudies-arrayexpress
Project description:Purpose: PKM2-mediated metabolic switch to aerobic glycolysis plays a critical role in promoting cell survival and proliferation. However, little is known about the function of intestinal epithelial PKM2 in intestinal homeostasis. Here we investigated whether and how intestinal epithelial PKM2 modulates the morphology and function of the adult intestine in experimental murine colitis. Methods: Colonoscopic biopsies from the Crohn’s disease (CD) and ulcerative colitis (UC) patients (10 each) were analyzed for PKM2 expression. We also generated intestinal epithelial-specific Pkm2 knockout mice and employed them to examine PKM2 function. Mouse intestinal inflammation was induced with dextran sulfate sodium (DSS) in drinking water. Disease phenotypes were investigated by mouse survival, body weight, colon length and analysis of immune cell infiltration in colon, intestinal epithelial cell gene profiling and signal pathway. Results: Intestinal epithelial PKM2 level in UC and CD patients was significantly decreased compared to that from non-inflamed intestinal epithelium. Similar reduction of intestinal epithelial PKM2 was observed in mice with experimental colitis. Supporting the notion that PKM2 serves as a safeguard against colitis, intestinal epithelial-specific Pkm2-deficient (Pkm2-/-) mice displayed a severer intestinal inflammation, companying with shortened colon, disruption of epithelial tight junction, higher permeability, elevation of inflammatory cytokines and immune cell infiltration, compared with wild-type mice. Gene profiling and western blot analysis indicated that cell survival signaling, particularly the Akt/β-catenin pathways, were downregulated in Pkm2-/- mice. Functional assay using mouse primary colonic epithelial cells confirmed that Pkm2 reduction decreased proliferation and migration of epithelial cells, while enhanced expression of Pkm2 was associated with increased transcriptional activity of β-catenin. Moreover, increasing mouse intestinal epithelial Pkm2 expression via delivery of Pkm2-expressing plasmid attenuated DSS-induced experimental colitis. Conclusions: Intestinal epithelial PKM2, through activating Wnt/β-catenin signaling, induces a strong proliferative and migratory response that increases cell survival and wound healing under colitic condition.
2018-08-20 | GSE118732 | GEO
Project description:That commensal bacteria can influence intestinal inflammation has been observed using other models of chronic colitis. Loss of IL-10, a major immunosuppressive cytokine, induces spontaneous colitis in mice. The incidence of spontaneous polyp formation in IL-10-deficient mice was also completely eliminated in the absence of STING We used microarrays to evaluate the inflammatory cytokine expression in the colon from IL10 KO mice and IL10/STING KO mice.
2018-02-01 | GSE107810 | 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:Metabolic dysregulation may serve as a pivotal driver of inflammatory bowel disease (IBD), with the crosstalk between metabolism and the immune system emerging as a critical research focus. Ulcerative colitis (UC) patients exhibit enhanced glycolysis but suppressed gluconeogenesis in the intestinal mucosa, yet the mechanistic links between these metabolic alterations and mucosal injury remain poorly defined. This study establishes phosphoenolpyruvate carboxykinase 1 (Pck1), a key rate-limiting enzyme in gluconeogenesis, as a central regulator of UC progression. We found Pck1 expression was significantly downregulated in colon tissues of UC patients and mice with DSS‑induced colitis. Utilizing an intestinal epithelial cell (IEC)-specific Pck1 knockout mouse model, we demonstrated for the first time that Pck1 deficiency exacerbates intestinal inflammation. Mechanistically, Pck1 depletion induces metabolic reprogramming that upregulates Pla2g6 expression, driving abnormal hydrolysis of phosphatidylcholine and phosphatidylethanolamine in IECs. Pharmacological inhibition of Pla2g6 ameliorated colitis in Pck1-deficient mice. These findings position Pck1 as a potential early diagnostic biomarker for UC and suggest that therapeutic targeting of the Pck1-Pla2g6 metabolic axis may yield novel strategies for UC management.
2025-05-07 | GSE296485 | GEO
Project description:Metabolic dysregulation may serve as a pivotal driver of inflammatory bowel disease (IBD), with the crosstalk between metabolism and the immune system emerging as a critical research focus. Ulcerative colitis (UC) patients exhibit enhanced glycolysis but suppressed gluconeogenesis in the intestinal mucosa, yet the mechanistic links between these metabolic alterations and mucosal injury remain poorly defined. This study establishes phosphoenolpyruvate carboxykinase 1 (Pck1), a key rate-limiting enzyme in gluconeogenesis, as a central regulator of UC progression. We found Pck1 expression was significantly downregulated in colon tissues of UC patients and mice with DSS‑induced colitis. Utilizing an intestinal epithelial cell (IEC)-specific Pck1 knockout mouse model, we demonstrated for the first time that Pck1 deficiency exacerbates intestinal inflammation. Mechanistically, Pck1 depletion induces metabolic reprogramming that upregulates Pla2g6 expression, driving abnormal hydrolysis of phosphatidylcholine and phosphatidylethanolamine in IECs. Pharmacological inhibition of Pla2g6 ameliorated colitis in Pck1-deficient mice. These findings position Pck1 as a potential early diagnostic biomarker for UC and suggest that therapeutic targeting of the Pck1-Pla2g6 metabolic axis may yield novel strategies for UC management.
2025-05-05 | GSE295845 | GEO
Project description:Group 2 innate lymphoid cells (ILC2) are enriched in colonic tissues, but their precise role under intestinal inflammation, including inflammatory bowel disease (IBD) other than helminth infection, is poorly understood. Here, we analysed global gene expression of colonic ILC2 in healthy and colitis mice and found that type I interferon (T1IFN)-stimulated genes (ISGs) are enriched in ILC2 under DSS-induced colitis. Enhancement of T1IFN signaling in ILC2 under DSS-induced colitis were correlated to downregulation in cytokine production of ILC2, such as IL-5. Blocking T1IFN signaling during colitis resulted in exaggeration of colitis both in wild-type and Rag2-deficient mice. Collectively, these findings show the potential roles of T1IFN in ILC2 contributing to the development of colitis.
2022-09-21 | GSE212939 | GEO
Project description:In adult mice the majority of intestinal macrophages exhibit a mature phenotype and are derived from blood monocytes. In the steady state replenishment of these cells is reduced in the absence of the chemokine receptor Ccr2. Within the intestine of mice with colitis there is marked increase in the accumulation of immature macrophages that demonstrate an inflammatory phenotype. However, whether Ccr2 is necessary for the accumulation of these immature macrophages and further for the development of colitis in susceptible mouse models is incompletely defined. Here, we ask whether Ccr2 is necessary for the development of colitis in mice lacking the receptor for IL10. We compared the development of intestinal inflammation in mice lacking IL10RA or both IL10RA and Ccr2. The absence of Ccr2 interfered with the accumulation of immature macrophages in IL10R-deficien mice, including a novel population of rounded submucosal Iba1+ cells and reduced the severity of colitis in these mice. In contrast, the absence of Ccr2 did not reduce augmented inflammatory gene expression observed in mature intestinal macrophages isolated from mice lacking IL10RA. These data suggest that both newly recruited Ccr2-dependent immature macrophages and Ccr2-independent residual mature macrophages contribute to the development of intestinal inflammation observed in IL10R-deficient mice.
2022-01-19 | GSE183960 | GEO