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.
2016-07-01 | E-GEOD-66938 | biostudies-arrayexpress
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.
2023-12-01 | GSE230139 | GEO
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.
2016-07-01 | GSE66938 | GEO
Project description:Mucus produced by goblet cells in the gastrointestinal (GI) tract forms a biological barrier that protects the intestine from invasion by commensals and pathogens. However, the host-derived regulatory network that controls mucus secretion and thereby changing gut microbiota has not been well studied. We found Forkhead box protein O1 (Foxo1) regulates mucus secretion by goblet cells and determines intestinal homeostasis. Loss of Foxo1 in intestinal epithelial cells (IECs) results in a defect in goblet cell autophagy and mucus secretion, leading to impaired gut microenvironment and dysbiosis.
2021-06-23 | GSE178650 | GEO
Project description:Remodeling of the gut microbiota is implicated in various metabolic and inflammatory diseases of the gastrointestinal tract. We hypothesized that the gut microbiota affects the DNA methylation profile of intestinal epithelial cells (IECs) which could, in turn, alter intestinal function. Here, we used mass spectrometry and methylated DNA capture to respectively investigate global and genome-wide DNA methylation of intestinal epithelial cells from germ-free (GF) and conventionally raised mice (CONV-R). In colonic IECs from GF mice, DNA was markedly hypermethylated. This was associated with a dramatic loss of Ten-Eleven-Translocation activity, a lower DNA methyltransferase activity and lower circulating levels of the one carbon metabolites cobalamin and folate. At the gene level, we found an enrichment for differentially methylated regions at proximity of genes regulating cytotoxicity of Natural Killer cells (FDR < 8.9E-6), notably members of the natural killer group 2 member D ligand superfamily Raet. Our results suggest that altered activity of methylation-modifying enzymes in GF mice influences the IEC epigenome at genes involved in the crosstalk between intestinal and immune cells. Epigenetic reprogramming of IECs by the gut microbiota may modulate intestinal function in diseases associated with altered gut microbiota.
2019-01-23 | GSE117434 | GEO
Project description:Despite accepted health benefits of dietary fiber, little is known about the mechanisms by which fiber deprivation impacts the gut microbiota and alters disease risk. Using a gnotobiotic model, in which mice were colonized with a synthetic human gut microbiota, we elucidated the functional interactions between dietary fiber, the gut microbiota and the colonic mucus barrier, which serves as a primary defence against pathogens. We show that during chronic or intermittent dietary fiber deficiency, the gut microbiota resorts to host-secreted mucus glycoproteins as a nutrient source, leading to erosion of the colonic mucus barrier. Dietary fiber deprivation promoted greater epithelial access and lethal colitis by the mucosal pathogen, Citrobacter rodentium, but only in the presence of a fiber-deprived microbiota that is pushed to degrade the mucus layer. Our work reveals intricate pathways linking diet, gut microbiome and intestinal barrier dysfunction, which could be exploited to improve health using dietary therapeutics. Germ-free mice (Swiss Webster) were colonized with synthetic human gut microbiota comprising of 14 species belonging to five different phyla (names of bacterial species: Bacteroides thetaiotaomicron, Bacteroides ovatus, Bacteroides caccae, Bacteroides uniformis, Barnesiella intestinihominis, Eubacterium rectale, Marvinbryantia formatexigens, Collinsella aerofaciens, Escherichia coli HS, Clostridium symbiosum, Desulfovibrio piger, Akkermansia muciniphila, Faecalibacterium prausnitzii and Roseburia intestinalis). These mice were fed either a fiber-rich diet or a fiber-free diet for about 6 weeks. The mice were then sacrificed and their cecal tissues were immediately flash frozen for RNA extraction. The extracted RNA was subjected to microarray analysis based on Mouse Gene ST 2.1 strips using the Affy Plus kit. Expression values for each gene were calculated using robust multi-array average (RMA) method.
2016-11-21 | GSE79067 | GEO
Project description:Wnt pathway-driven proliferation and renewal of the intestinal epithelium must be tightly controlled to prevent development of cancer and barrier dysfunction. Although type 1 interferons (IFN) produced in the gut under influence of microbiota are known for their anti-proliferative effects, the role of these cytokines in regulating intestinal epithelial renewal is largely unknown. Here we report a novel role for IFN in the context of intestinal knockout of casein kinase 1α (CK1α), which controls ubiquitination and degradation of both β-catenin and the IFNAR1 chain of the IFN receptor. Ablation of CK1α leads to activation of both β-catenin and IFN pathway and prevents unlimited proliferation of intestinal epithelial cells despite constitutive β-catenin activity. IFN signaling contributes to activation of the p53 pathway and appearance of apoptotic and senescence markers in the CK1α-deficient gut. Concurrent genetic ablation of CK1α and IFNAR1 leads to intestinal hyperplasia, robust attenuation of apoptosis, and rapid and lethal loss of the barrier function. These data indicate that IFN plays an important role in controlling proliferation and function of intestinal epithelium in the context of β-catenin activation. Two conditions were examined, with 2 replicates for each condition, yielding 4 samples in total.
2016-01-05 | E-GEOD-76512 | biostudies-arrayexpress
Project description:To gain insight into host-microbe interactions in a piglet model, a functional genomics approach has been applied to address the working hypothesis that transcriptionally regulated genes associated with promoting epithelial barrier function evolved as a defensive response to the intestinal microbiota. Cesarean-derived germfree (GF) newborn piglets were colonized with adult swine feces, and villus and crypt epithelial cell transcriptomes from colonized and GF neonatal piglets were compared using laser-capture microdissection and high-density porcine oligonucleotide microarray technology. Consistent with our hypothesis, results revealed that resident microbiota induces the expression of genes encoding proteins involved in promoting intestinal epithelial cell turnover and mucus biosynthesis and priming of the immune system. Furthermore, differential expression of genes associated with antigen presentation (SLA-7, B2M, TAP1 and TAPBP) demonstrates that microbiota induced immune responses using a distinct regulatory mechanism common for these genes. Intestinal microbiota stimulated interferon (IFN) receptor-mediated signaling cascade using signal transducer and activator of transcription-1 (STAT1), STAT2 and IFN regulatory factor-7 transcription factors to activate IFN-inducible genes. In addition, excessive inflammatory responses were prevented by activating RNA expression of inhibitory-kappa-B and Toll-interacting protein, along with downregulating the expression of a gene encoding GATA binding protein-1 consistent with the maintenance of intestinal homeostasis. This study supports the concept that the intestinal epithelium has evolved to maintain a physiological state of inflammation with respect to continuous microbial exposure, which serves to maintain tight intestinal barrier but prevent overt inflammatory responses that would compromise barrier function. Keywords: oligonucleotide array
2008-03-04 | GSE7232 | GEO
Project description:Sepsis, a critical organ dysfunction resulting from an aberrant host response to infection, remains a leading cause of mortality in ICU patients. Recent evidence suggests that angiotensin converting enzyme 2 (ACE2) contributes to intestinal barrier function, the mechanism of which is yet to be explored. The findings of this study indicate that ACE2 shedding significantly weakens the integrity of the intestinal barrier in septic conditions. Mice lacking ACE2 exhibited increased intestinal permeability and higher mortality rates post-sepsis compared to their wild-type counterparts. Notably, ACE2 deficiency was associated with distinct alterations in gut microbiota composition and reductions in protective metabolites, such as 5-methoxytryptophan (5-MTP). 5-MTP was barely detected in ABX mice, while its level was reversed by FMT of WT mice. Supplementing septic mice with 5-MTP ameliorated gut leak through enhanced epithelial cell proliferation and repairment. The relationship between intestinal barrier integrity and the expression of ACE2 in septic mice was explored in both ACE2 knockout and overexpressing mice. Intestinal barrier function was assessed through measurements of intestinal tight junction proteins and permeability tests. The resulting bacteria translocation and multi-organ dysfunction were also evaluated.
2025-06-04 | GSE267002 | GEO
Project description:<p><strong>BACKGROUND:</strong> Dietary intervention has been reported to improve intestinal health. The intestinal microbiota of newborn animals plays a fundamental role in the development of intestinal function and the innate immune system. However, little is currently known about dietary interventions in the gut microbiota and barrier function of livestock, especially suckling Bamei piglets. To this end, we studied the effect of early dietary supplementation on intestinal bacterial communities and intestinal barrier function in piglets.</p><p><strong>RESULTS:</strong> 10 purebred Bamei sows were randomly allocated into two groups. In group one, the piglets received a supplementary milk replacer on day 7 of age, whereas the other control group was allowed sow’s milk alone. At 21 days, 18 and 17, respectively, piglets in each group of average weight were randomly selected and sacrificed. Tissue and digesta samples were collected from the jejunum to evaluate differences in the microbiome-metabolome and the mRNA expression of inflammatory cytokines (TLR4, TNFα and IL-8) and barrier proteins (ZO-1, Occludin and Claudin-1). Sequencing of 16S rRNA revealed that ES improved the gut microbiome composition of Bamei suckling piglets. The relative abundances of some bacterial species such as Lactobacillales, Romboutsia, Actinobacillus, Bacteroides were significantly reduced in the ES group. Metabolomics analysis indicated that 23 compounds were enriched and 35 compounds decreased in the ES group. And correlation analysis demonstrated that some gut bacterial genera were highly correlated with altered gut microbiota-related metabolites. Meanwhile, ES of Bamei suckling piglets altered the gene expression of inflammatory cytokine and barrier protein in the jejunum.</p><p><strong>CONCLUSIONS:</strong> In summary, these results provide important insights on the relationships between jejunal microbiota and related metabolites, and jejunal barrier function during the early life of Bamei suckling piglets.</p>
2020-06-05 | MTBLS1698 | MetaboLights