Pig gut metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA297060 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2601043.fastq.gz | Fastqsanger.gz |
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Project description:Gut dysbiosis is closely involved in the pathogenesis of inflammatory bowel disease (IBD). However, it remains unclear whether IBD-associated gut dysbiosis plays a primary role in disease manifestation or is merely secondary to intestinal inflammation. Here, we established a humanized gnotobiotic (hGB) mouse system to assess the functional role of gut dysbiosis associated with two types of IBD - Crohn's disease (CD) and ulcerative colitis (UC). In order to explore the functional impact of dysbiotic microbiota in IBD patients on host immune responses, we analyzed gene expression profiles in colonic mucosa of hGB mice colonized with healty (HC), CD, and UC microbiota.
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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:Gut microbiota modulation has emerged as a potential therapeutic and diagnostic approach for inflammatory bowel disease (IBD). We generated transcriptomic data by Record-seq, a method based on CRISPR-Cas system, that enables recording of gene expression in reporter bacteria within the mouse gut.
2025-07-22 | GSE303196 | GEO
Project description:Human and piglet gut microbiota Raw sequence reads
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Project description:An early settlement of a complex gut microbiota can protect against gastro-intestinal dysbiosis, but the effects of neonatal microbiota colonization on the gut barrier upon the further encounter of favorable bacteria or not, are largely unknown. The jejunal transcriptome of differently perfused intestinal loops of 12 caesarian-derived pigs previously associated with microbiota of different complexity was studied. Pigs received pasteurized sow colostrum at birth (d0), 2 mL of starter microbiota (10^7 CFU of each Lactob. Amylovorus (LAM), Clostr. glycolicum, and Parabacteroides spp.) on d1-d3 of age and either a placebo inoculant (simple association, SA) or an inoculant consisting of diluted feces of an adult sow (complex association, CA) on d3-d4 of age. On days 26-37 of age, jejunal loops were perfused for 8 h with either enterotoxigenic E. coli F4 (ETEC), F4 fimbriae (F4), LAM or saline (CTRL) and jejunal samples were obtained from each piglet immediately afterwards. The analysis of whole mRNA transcript expression was done by Affymetrix©Porcine Gene 1.1 ST array strips, a Robust Multichip Analysis was performed on the CEL files, and Transcripts IDâs were associated to 13,406 Human gene names, based on Sus scrofa Ensemble
2016-02-11 | E-GEOD-77787 | biostudies-arrayexpress
Project description:Abstract. Background: The cause of ulcerative colitis (UC) is not yet fully understood. Previous research has pointed towards a potential role for mutations in NOD2 in promoting the onset and progression of inflammatory bowel disease (IBD) by altering the microbiota of the gut. However, the relationship between toll-like receptor 4 (TLR4) and gut microbiota in IBD is not well understood. To shed light on this, the interaction between TLR4 and gut microbiota was studied using a mouse model of IBD. Methods: To examine the function of TLR4 signaling in intestinal injury repair, researchers developed Dextran Sulfate Sodium Salt (DSS)-induced colitis and injury models in both wild-type (WT) mice and TLR4 knockout (TLR4-KO) mice. To assess changes in the gut microbiota, 16S rRNA sequencing was conducted on fecal samples from both the TLR4-KO and WT enteritis mouse models. Results: The data obtained depicted a protective function of TLR4 against DSS-induced colitis. The gut microbiota composition was found to vary considerably between the WT and TLR4-KO mice groups as indicated by β-diversity analysis and operational taxonomic units (OTUs) cluster. Statistical analysis of microbial multivariate variables depicted an elevated abundance of Escherichia coli/Shigella, Gammaproteobacteria, Tenerlcutes, Deferribacteres, Enterobacteria, Rikenellaceae, and Proteobacteria in the gut microbiota of TLR4-KO mice, whereas there was a considerable reduction in Bacteroidetes at five different levels of the phylogenetic hierarchy including phylum, class, order, family, and genus in comparison with the WT control. Conclusion: TLR4 may protect intestinal epithelial cells from damage in response to DSS-induced injury by controlling the microbiota in the gut.
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