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Mouse gut metagenome

ABSTRACT: 16S rDNA Amplicon Sequencing of gut microbiota in mice

PROVIDER: PRJNA745400 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15178914_1.fastq.gz	Fastqsanger.gz
	SRR15178914_2.fastq.gz	Fastqsanger.gz
	SRR15178915_1.fastq.gz	Fastqsanger.gz
	SRR15178915_2.fastq.gz	Fastqsanger.gz
	SRR15178916_1.fastq.gz	Fastqsanger.gz

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Project description:Introduction: Chronic sleep fragmentation (SF) is prevalent in contemporary human society, highlighting detrimental effects on glucose metabolism and adipose tissue morphology, which is closely linked to gut microbiota composition. However, it remains unclear whether sleep recovery (SR) after prolonged SF can ameliorate glucose metabolism, influence the transcriptome of inguinal white adipose tissue (iWAT), and whether these effects align with alterations in the gut microbiota. Methods: Mice were subjected to 8 weeks of SF and subsequently allowed 2 weeks of SR. We assessed glucose tolerance through intraperitoneal glucose tolerance tests (ipGTT), analyzed gut microbiota via 16s rDNA amplicon sequencing, and examined transcriptomic alterations in iWAT using RNA sequencing. Results: Despite the two-week SR following chronic SF, significant glucose intolerance persisted, accompanied by subtle shifts in the gut microbiota and alterations in gene expression within iWAT. The top hub genes Ncapg, Cenpe, and Tik were identified from the protein-protein interaction network. Conclusion: Even followed by a brief period of SR, prolonged SF still led to ongoing glucose intolerance and alterations in the adipose tissue transcriptome in mice. These changes were intertwined with modifications in the gut microbiome. The shifts in gut microbiota may play a pivotal role in understanding the sustained negative effects of SF.

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Project description:Advanced age is associated with chronic low-grade inflammation, which is usually referred to as inflammaging. Elderly are also known to have an altered gut microbiota composition. However, whether inflammaging is a cause or consequence of an altered gut microbiota composition is not clear. In this study gut microbiota from young or old conventional mice was transferred to young germ-free mice. Four weeks after gut microbiota transfer immune cell populations in spleen, Peyer’s patches, and mesenteric lymph nodes from conventionalized germ-free mice were analyzed by flow cytometry. In addition, whole-genome gene expression in the ileum was analyzed by microarray. Gut microbiota composition of donor and recipient mice was analyzed with 16S rDNA sequencing. Here we show by transferring aged microbiota to young germ-free mice that certain bacterial species within the aged microbiota promote inflammaging. This effect was associated with lower levels of Akkermansia and higher levels of TM7 bacteria and Proteobacteria in the aged microbiota after transfer. The aged microbiota promoted inflammation in the small intestine in the germ-free mice and enhanced leakage of inflammatory bacterial components into the circulation was observed. Moreover, the aged microbiota promoted increased T cell activation in the systemic compartment. In conclusion, these data indicate that the gut microbiota from old mice contributes to inflammaging after transfer to young germ-free mice.

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