Ontology highlight
ABSTRACT:
PROVIDER: PRJNA760658 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15729400_1.fastq.gz | Fastqsanger.gz | |||
| SRR15729400_2.fastq.gz | Fastqsanger.gz | |||
| SRR15729401_1.fastq.gz | Fastqsanger.gz | |||
| SRR15729401_2.fastq.gz | Fastqsanger.gz | |||
| SRR15729402_1.fastq.gz | Fastqsanger.gz |
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Project description:The impact of dietary proteins on homeostasis and immune function of the intestine is poorly understood. We here show that physiological uptake of dietary proteins induced an activated, CD4+CD44+Helios+ T cell population, predominantly in Peyer's patches (PP). These cells are distinct from Foxp3+regulatory T cells and microbiota-independent. Dietary protein-reactive T lymphocytes remained innocuous due to an equilibrium between activation and apoptosis. Macrophage mediated uptake of apoptotic T cells from the PP but not from other tissues resulted in strong IL-10 expression. In contrast, replacement of dietary proteins by amino acids resulted in low numbers of activated and apoptotic CD4+CD44+Helios+ T cells together with reduced amounts of IL-10 and downregulation of genes involved in intestinal integrity such as trefoil factors and gastrokines. The impaired intestinal barrier function of these animals was restored after switching to conventional diet, demonstrating the essential role of food proteins for induction of epithelial repair mechanisms and immunological homeostasis. Microarray experiments were performed as dual-color hybridizations on Agilent-014868 Whole Mouse Genome 4x44K catalog arrays. To compensate for dye-specific effects, a dye-reversal color-swap was applied.
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Project description:A diet rich in dietary fiber and polyphenols supports the normal intestinal barrier function crucial for intestinal and overall health. Birch wood-derived fiber containing glucuronoxylans (GX)- and polyphenols have the potential in multiple food technological applications and have favorable effects on gut microbiota and colonic metabolism. However, their impact on intestinal barrier function is unknown. To elucidate their potential as new intestinal health-supporting food ingredients, we investigated the effect of GX- and polyphenol-rich extract (GXpoly ) and highly purified GX-rich extract (pureGX) on the gene expression of the colon mucosa.
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Project description:A striking example of the intricate interplay between diet, microbiota, and host is the effect of inulin, a dietary fiber, on the intestinal epithelium. Ingestion of inulin triggers a wide range of epithelial effects in the colon, such as enhanced proliferation, increased production of mucus and antimicrobial peptides, as well as systemic effects on host metabolism and immune function that are dependent on microbiota-derived molecules. In this study, we investigated the impact of inulin on two critical aspects of diet-microbiota-host interactions: intestinal hypoxia and the modulation of hypoxia-inducible factor (HIF)-1 signaling in intestinal epithelial cells (IECs) in mice colon. To achieve this, we employed a multilayered and multi-omics approach, including dietary interventions, in vitro analysis using intestinal organoids, and both genetic and pharmacological interventions. We found that inulin intake enhances intestinal hypoxia, resulting in the stabilization of HIF-1 in IECs, an effect that is both microbiota- and host-dependent. Our study revealed that HIF-1 plays a key role in regulating IEC proliferation and intestinal stem cell (ISC) function. These changes are associated with HIF-1-dependent metabolic alterations in IECs. Our findings uncover a novel mechanism by which HIF-1 acts in the colon: it acts as a molecular brake, modulating cell proliferation in a microbiota-dependent manner and through metabolic reprogramming, highlighting the complexity of the diet-microbiota-host interactions in the gut.
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Project description:The intestinal epithelium, a self-renewing single-cell layer, acts as a physical barrier isolating gut microbiota from deeper tissues. In human IBD and experimental IBD mouse models, this barrier is compromised, causing microbial infiltration and inflammation. However, the pathogenesis of IBD remains to be fully understood. Our research shows that the absence of TRMT6 in the mouse gut impairs the intestinal mucosal barrier, increasing susceptibility to DSS-induced colitis. Mechanically, loss of TRMT6 in intestinal epithelial cells disrupts m¹A modification-mediated translational control and impairs MYC protein synthesis–a deficiency that inhibits epithelial cell proliferation and differentiation. Further multi-omics analyses suggest that TRMT6 deficiency may be associated with perturbations in intestinal lipid metabolism, nutrient absorption, metabolite homeostasis, and gut microbiota composition–changes that could collectively contribute to the acceleration of colitis progression. In summary, TRMT6 is crucial for maintaining small intestinal mucosal barrier function, offering insights into how its deficiency may drive gastrointestinal inflammation in IBD. Given the critical role of TRMT6 in maintaining intestinal homeostasis, our findings highlight its potential as a therapeutic target for IBD treatment.
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Project description:The intestinal epithelium, a self-renewing single-cell layer, acts as a physical barrier isolating gut microbiota from deeper tissues. In human IBD and experimental IBD mouse models, this barrier is compromised, causing microbial infiltration and inflammation. However, the pathogenesis of IBD remains to be fully understood. Our research shows that the absence of TRMT6 in the mouse gut impairs the intestinal mucosal barrier, increasing susceptibility to DSS-induced colitis. Mechanically, loss of TRMT6 in intestinal epithelial cells disrupts m¹A modification-mediated translational control and impairs MYC protein synthesis–a deficiency that inhibits epithelial cell proliferation and differentiation. Further multi-omics analyses suggest that TRMT6 deficiency may be associated with perturbations in intestinal lipid metabolism, nutrient absorption, metabolite homeostasis, and gut microbiota composition–changes that could collectively contribute to the acceleration of colitis progression. In summary, TRMT6 is crucial for maintaining small intestinal mucosal barrier function, offering insights into how its deficiency may drive gastrointestinal inflammation in IBD. Given the critical role of TRMT6 in maintaining intestinal homeostasis, our findings highlight its potential as a therapeutic target for IBD treatment.
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