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Dextran sulfate sodium (DSS)-induced colitis in WT and NAPRT KO mice [scWT2]

ABSTRACT: NAPRT-mediated deamidated biosynthesis of nicotinamide adenine dinucleotide (NAD), an essential electron carrier for hundreds of biochemical reactions in all living cells, mediates the diet-microbe-host NAD metabolic interaction in mice. To study the function of this metabolic pathway in vivo, we recently generated a mutant mouse strain (NAPRT KO) in which a 21-nt fragment that encodes 7 amino acids in the catalytic domain of NAPRT was deleted in all cells using the CRISPR/Cas9-mediated gene editing technology. Our data showed that NAPRT KO mice are hypersensitive to DSS-induced colitis. To better understand this hypersensitivity at the molecular level, we analyzed transcriptomes of colon tissues from DSS-treated WT and NAPRT KO mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE271836 | GEO | 2025/12/06

REPOSITORIES: GEO

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Dextran sulfate sodium (DSS)-induced colitis in WT and NAPRT KO mice [NAPRTKODSS]

Project description:NAPRT-mediated deamidated biosynthesis of nicotinamide adenine dinucleotide (NAD), an essential electron carrier for hundreds of biochemical reactions in all living cells, mediates the diet-microbe-host NAD metabolic interaction in mice. To study the function of this metabolic pathway in vivo, we recently generated a mutant mouse strain (NAPRT KO) in which a 21-nt fragment that encodes 7 amino acids in the catalytic domain of NAPRT was deleted in all cells using the CRISPR/Cas9-mediated gene editing technology. Our data showed that NAPRT KO mice are hypersensitive to DSS-induced colitis. To better understand this hypersensitivity at the molecular level, we analyzed transcriptomes of colon tissues from DSS-treated WT and NAPRT KO mice.

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Project description:Dextran sulfate sodium (DSS)-induced colitis in WT and NAPRT KO mice [scWT2]

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Dextran sulfate sodium (DSS)-induced colitis in WT and NAPRT KO mice [NAPRTKODSS]

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Project description:Ulcerative colitis (UC) is an intestinal pathology characterized by chronic recurrent inflammation, which requires in-depth exploration of its mechanisms. To investigate the biological effects of TLR2 on DSS-induced intestinal inflammation in mice, we constructed the WT and TLR2-KO colitis mice model. We found TLR2-KO mice were severely susceptible to DSS-induced colitis. To determine how TLR2 exerted a protective effect in DSS-induced colitis, we compared the global gene expression profiles in the gut between WT and TLR2-KO mice by RNA-Seq. Results suggested that cell cycle pathway-related genes were significantly downregulated in gut of TLR2-KO colitis mice. 16S rRNA gene sequencing demonstrated remarkable variation in the composition of gut microbiota between WT and TLR2-KO colitis mice. Compared with WT colitis mice, the relative abundance of Marinifilaceae, Rikenellaceae, Desulfovibrionaceae, Tannerellaceae, Ruminococcaceae, Clostridia, Mycoplasmataceae were significantly higher in the gut of TLR2-KO colitis mice at family level. Moreover, we found that the relative abundance of Marinifilaceae was negatively correlated with the expression of cell cycle signaling related genes by microbiome diversity-transcriptome collaboration analysis. We came to this conclusion: TLR 2-KO exacerbated DSS-induced intestinal injury by Marinifilaceae dependent attenuating cell cycle signaling.

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