DSS mouse gut bacterial communities
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA911821 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22815100.fastq.gz | Fastqsanger.gz | |||
| SRR22815200.fastq.gz | Fastqsanger.gz | |||
| SRR22815101.fastq.gz | Fastqsanger.gz | |||
| SRR22815201.fastq.gz | Fastqsanger.gz | |||
| SRR22815102.fastq.gz | Fastqsanger.gz |
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Project description:Abstract. Ulcerative colitis (UC) is an intestinal disease characterized by chronic recurrent inflammation, but the underlying mechanism remains undefined and requires in-depth exploration. The aim of the present study was to investigate the biological effects of a small molecular compound M1002 of oxygen-sensing signaling pathway on dextran sulfate sodium (DSS)-induced intestinal inflammation colitis mouse models. It was found that the protective effects of M1002 on DSS-induced colitis. To determine how M1002 exerted its protective effect in DSS-induced colitis, we compared the global gene expression profiles in the gut between DSS control and M1002 treatment colitis mouse groups by RNA-Seq. The results demonstrated that HIF-1 signaling pathway-related genes were significantly upregulated in the gut of M1002 treatment colitis mice, whereas the Inflammatory bowel disease signaling pathway, the TNF signaling pathway, and Cytokines and inflammatory response signaling pathway related genes were significantly downregulated in the M1002 treatment group. 16S rRNA gene sequencing demonstrated remarkable variations in the composition of gut microbiota between DSS control and M1002 treatment colitis mice. Compared with DSS control colitis mice, the relative abundance of Eubacterium_nodatum and Halomonas in the gut microbiota was significantly increased at genus level in the gut of M1002 treatment colitis mice. Based on these findings, we tend to conclude that M1002 might alleviate DSS-induced gut injury in mice by regulation of HIF-1 signaling and up-regulating Eubacterium_nodatum and Halomonas.
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Project description:Investigation of microbial community composition in mouse models using an intestinal epithial-specific and inducible VilCreERT2-mediated conditional knockout of Jup under basal conditions and in acute dextran-sodium sulfate (DSS)-induced colitis We investigated the gut microbiome composition in a dextran sulfate sodium (DSS) colitis model using Jupfl/fl and iVilCreERT2Jupfl/fl mice. Fecal samples were collected after DSS treatment, and 16S rRNA sequencing was employed to analyze microbial communities. Our findings revealed no significant differences in microbial profiles between Jupfl/fl and iVilCreERT2Jupfl/fl under DSS treatment.
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Project description:mouse gut bacterial metagenome Raw sequence reads
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Project description:The host genotype has been proposed to contribute to individually composed bacterial communities in the gut. To provide deeper insight into interactions between gut bacteria and their host, we associated germ-free C3H and C57BL/10 mice with intestinal bacteria from a C57BL/10 donor mouse. Analysis of microbiota similarity between the experimental animals with denaturing gradient gel electrophoresis (DGGE) 13 weeks after association revealed the development of a mouse strain specific microbiota. Gene expression in the colonic mucosa was analyzed with a microarray approach taking advantage of a modified Affymetrix mouse genome chip. We detected 202 genes whose expression differed significantly by a factor of < 2. Application of bioinformatics tools demonstrated that functional terms including signaling/secretion, lipid degradation/catabolism, guanine nucleotide/guanylate binding and immune response were significantly enriched in differentially expressed genes. We had a closer look at the 56 genes with expression differences of < 4 and observed a higher expression in C57BL/10 mice of the genes coding for toll-like receptor 1 (4-fold) and angiogenin 4 (33-fold) which are involved in the recognition and response to gut bacteria. In contrast, a 70-fold higher expression of the phospholipase A2, group IIA-encoding gene (Pla2g2a) was detected in C3H mice. In addition, a number of interferon-inducible genes were higher expressed in C3H than in C57BL/10 mice including Gbp1 (18-fold), Mal (7-fold), Oasl2 (7-fold), Ifi202b (7-fold), Rtp4 (6-fold), Ly6g6c (5-fold), Ifi27l2a (5-fold), Usp18 (5-fold), Ifit1 (5-fold), Ifi44 (4-fold), and Ly6g (4-fold) indicating that these cytokines play an essential role in microbiota regulation. However, genes coding for interferons, their receptors or factors involved in interferon signaling pathways were not differentially expressed between the two mouse strains. Taken together, our study confirms that the host genotype is involved in the establishment of host-specific bacterial communities in the gut. Based on expression differences after colonization with the same bacterial inoculum, we propose that Pla2g2a and interferon-dependent genes may contribute to this phenomenon. Total RNA was extracted from the colonic mucosa and hybridization was performed using 12.5M-BM- M-bM-^@M-^SM-BM- 20M-BM- M-BM-5g of cDNA on a customized Affymetrix nugomm 1a520177 chip.
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Project description:We quantitatively examine inputs and outputs of the mouse gut microbiome, using isotope tracing. To determine nutrient preferences across bacteria, we traced into genus-specific bacterial protein sequences. By in vivo isotope tracer feeding, mapped the contribution of different dietary nutrients vs circulating nutrients contribution to different gut bacterial genera.
2022-08-17 | PXD031015 | Pride
Project description:The host genotype has been proposed to contribute to individually composed bacterial communities in the gut. To provide deeper insight into interactions between gut bacteria and their host, we associated germ-free C3H and C57BL/10 mice with intestinal bacteria from a C57BL/10 donor mouse. Analysis of microbiota similarity between the experimental animals with denaturing gradient gel electrophoresis (DGGE) 13 weeks after association revealed the development of a mouse strain specific microbiota. Gene expression in the colonic mucosa was analyzed with a microarray approach taking advantage of a modified Affymetrix mouse genome chip. We detected 202 genes whose expression differed significantly by a factor of < 2. Application of bioinformatics tools demonstrated that functional terms including signaling/secretion, lipid degradation/catabolism, guanine nucleotide/guanylate binding and immune response were significantly enriched in differentially expressed genes. We had a closer look at the 56 genes with expression differences of < 4 and observed a higher expression in C57BL/10 mice of the genes coding for toll-like receptor 1 (4-fold) and angiogenin 4 (33-fold) which are involved in the recognition and response to gut bacteria. In contrast, a 70-fold higher expression of the phospholipase A2, group IIA-encoding gene (Pla2g2a) was detected in C3H mice. In addition, a number of interferon-inducible genes were higher expressed in C3H than in C57BL/10 mice including Gbp1 (18-fold), Mal (7-fold), Oasl2 (7-fold), Ifi202b (7-fold), Rtp4 (6-fold), Ly6g6c (5-fold), Ifi27l2a (5-fold), Usp18 (5-fold), Ifit1 (5-fold), Ifi44 (4-fold), and Ly6g (4-fold) indicating that these cytokines play an essential role in microbiota regulation. However, genes coding for interferons, their receptors or factors involved in interferon signaling pathways were not differentially expressed between the two mouse strains. Taken together, our study confirms that the host genotype is involved in the establishment of host-specific bacterial communities in the gut. Based on expression differences after colonization with the same bacterial inoculum, we propose that Pla2g2a and interferon-dependent genes may contribute to this phenomenon.
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