Human feces
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ABSTRACT:
PROVIDER: PRJNA842201 | ENA |
REPOSITORIES: ENA
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Project description:Gut microbiota after dietary intervention
| PRJNA202975 | ENA
Project description:Feces 16s rRNA seq experiments is required to demonstrate the AZ1 doesn’t impact the intestinal microbiota.
2020-02-14 | GSE143003 | GEO
Project description:Development of immune competence in pigs is important for resilience, disease resistance, and performance later in life. Dietary interventions in early life can contribute to immune system development. Use of model dietary interventions, such as diets with a high concentration of zinc, can contribute to the understanding of the interactions between the diet, the intestinal microbiota and intestinal tissues. The aim of the present study was to evaluate the effects of provision of a diet with a high concentration of zinc (Zn, 2690 mg/kg), as model intervention, as compared to provision of a control diet with a regular Zn concentration (100 mg/kg) during a period of nine days during the post weaning period (d 14-23 post weaning (pw)), on the composition of the intestinal microbiota and gene expression in the intestinal mucosa on d 23 and 35 pw (12 d after the termination of the Zn intervention). Whole genome gene expression analysis of the jejunal and ileal mucosa revealed a small overall time-treatment interaction effect at d 23 pw in both intestinal tissues. In both jejunal and ileal mucosa various genes/probes were differentially up or down regulated between treatments. In intestinal tissue samples obtained on d 35 no differences in gene expression were observed. Probes of d 23 pw that were differently expressed and had an annotation were subsequently used as input for further functional analysis using DAVID and Gene Decks databases. The analysis did not result in the identification of gene sets that were differentially expressed between dietary treatments. However, it was shown that a number of upregulated genes in the jejunal mucosa on d 23 pw by the high zinc intervention are involved in pathways related to mineral absorption, immune signalling and cell energy metabolism (glycolysis and gluconeogenesis). A few down regulated genes by the Zn intervention are also involved in immune signalling pathways. It was concluded from the present study that provision of a diet with a high concentration of zinc as zinc oxide during a short period of time (9 days) to piglets in the post weaning period (d 14-23 pw) induces differences on the intestinal expression of genes in part related to the functioning of the local innate immune system. The high dietary zinc intervention can therefore be considered as a suitable model for studying relationships between dietary interventions and development of immune competence in post weaning piglets.
2017-04-19 | GSE94370 | GEO
Project description:Colorectal cancer (CRC) is closely related to gut dysbiosis. We investigated the effects of imbalanced gut microbiota on the progression of intestinal adenoma in Apcmin/+ mice model using fecal microbiota transplantation (FMT). Administration of feces from CRC patients increased tumor proliferation and decreased apoptosis in tumor cells. Abnormal expression of genes related to Wnt-protein binding and lipid metabolic process was observed.
2019-09-16 | GSE136682 | GEO
Project description:Arginase 1 (Arg1), which converts L-arginine into ornithine and urea, exerts pleiotropic immunoregulatory effects. Patients with inflammatory bowel disease (IBD) show an enhanced expression and activity of Arg1 in the intestinal (sub-)mucosa, but the function of Arg1 in IBD remains poorly characterized. Here, we found that Arg1 expression correlates with the degree of inflammation in colitic tissues of IBD patients. In mice with - experimental colitis Arg1 was upregulated in an IL-4-/IL-13- and intestinal microbiota-dependent manner. Tie2-Cre+/-Arg1fl/fl mice lacking Arg1 in hematopoietic and endothelial cells recovered faster from colitis than Arg1-expressing littermates. This correlated with decreased vessel density, compositional changes in the intestinal microbiota, diminished infiltration by myeloid cellsand an accumulation of intraluminal polyamines that are associated with epithelial healing. Dietary L-arginine restriction abolished the protective effect of Arg1-deletion, suggesting that protection is related to an increased availability of L-arginine. Fecal microbiota transfers from Tie2-Cre+/-Arg1fl/fl mice into wildtype recipients restored the protective, anti-inflammatory phenotype while transfers from wildtype littermates into Arg1-deficient mice prevented the accelerated recovery from colitis. Thus, altered intestinal microbiota and metabolic products in Tie2-Cre+/-Arg1fl/fl mice account for the accelerated resolution from colitis in the absence of Arg1. Subsequently, L-arginine serves as novel therapeutic and diagnostic target for clinical intervention in IBD patients.
2020-06-07 | GSE151931 | GEO
Project description:Purpose: Helminth infection and dietary intake can affect the intestinal microbiota, as well as the immune system. Methods: Here we analyzed the relationship between fecal microbiota and blood profiles of indigenous Malaysians, referred to locally as Orang Asli, in comparison to urban participants from the capital city of Malaysia, Kuala Lumpur. Results: We found that helminth infections had a larger effect on gut microbial composition than did dietary intake or blood profiles. Trichuris trichiura infection intensity also had the strongest association with blood transcriptional profiles. By characterizing paired longitudinal samples collected before and after deworming treatment, we determined that changes in serum zinc and iron levels among the Orang Asli were driven by changes in helminth infection status, independent of dietary metal intake. Serum zinc and iron levels were associated with changes in the abundance of several microbial taxa. Conclusions: There is considerable interplay between helminths, micronutrients and the microbiota on the regulation of immune responses in humans.
2019-10-01 | GSE137338 | GEO
Project description:Gut microbiota has profound effects on obesity and associated metabolic disorders. Targeting and shaping the gut microbiota via dietary intervention using probiotics, prebiotics and synbiotics can be effective in obesity management. Despite the well-known association between gut microbiota and obesity, the microbial alternations by synbiotics intervention, especially at the functional level, are still not characterized. In this study, we investigated the effects of synbiotics on high fat diet (HFD)-induced metabolic disorders, and systematically profiled the microbial profile at both the phylogenetic and functional levels. Synbiotics significantly reversed the HFD-induced change of microbial populations at the levels of richness, taxa and OTUs. Potentially important species Faecalibaculum rodentium and Alistipes putredinis that might mediate the beneficial effects of synbiotics were identified. At the functional level, short chain fatty acid and bile acid profiles revealed that interventions significantly restored cecal levels of acetate, propionate, and butyrate, and synbiotics reduced the elevated total bile acid level. Metaproteomics revealed the effect of synbiotics might be mediated through pathways involved in carbohydrate, amino acid, and energy metabolisms, replication and repair, etc. These results suggested that dietary intervention using our novel synbiotics alleviated HFD-induced weight gain and restored microbial ecosystem homeostasis phylogenetically and functionally.
2022-02-22 | PXD009564 | Pride
Project description:Mild or transient dietary restriction (DR) improves many aspects of health and aging. Emerging evidence from us and others has demonstrated that DR also optimizes the development and quality of immune responses. However, the factors and mechanisms involved remain to be elucidated. Here, we demonstrate that DR-induced optimization of immunological memory requires co-operation between memory T cells, the intestinal microbiota, and myeloid cells. Our data indicate that DR enhances the ability of memory T cells to recruit and activate myeloid cells in the context of a secondary infection. Concomitantly, DR promotes expansion of the commensal Bifidobacteria within the large intestine, which supplies the short-chain fatty acid acetate to myeloid cells. Acetate conditioning of the myeloid compartment during DR enhances their capacity to kill pathogens. Enhanced host protection during DR is abolished when Bifidobacteria expansion is prevented, indicating that microbiota configuration and function critically dictates immune responsiveness to this dietary intervention. Altogether, DR induces both memory T cells and the gut microbiota to produce essential, distinct factors that converge on myeloid cells to promote optimal pathogen control. These findings reveal how nutritional cues promote adaptation and co-operation between multiple immune cells and the gut microbiota, which synergize to optimize immunity and protect the collective metaorganism.
2024-02-21 | GSE223739 | GEO
Project description:Mild or transient dietary restriction (DR) improves many aspects of health and aging. Emerging evidence from us and others has demonstrated that DR also optimizes the development and quality of immune responses. However, the factors and mechanisms involved remain to be elucidated. Here, we demonstrate that DR-induced optimization of immunological memory requires co-operation between memory T cells, the intestinal microbiota, and myeloid cells. Our data indicate that DR enhances the ability of memory T cells to recruit and activate myeloid cells in the context of a secondary infection. Concomitantly, DR promotes expansion of the commensal Bifidobacteria within the large intestine, which supplies the short-chain fatty acid acetate to myeloid cells. Acetate conditioning of the myeloid compartment during DR enhances their capacity to kill pathogens. Enhanced host protection during DR is abolished when Bifidobacteria expansion is prevented, indicating that microbiota configuration and function critically dictates immune responsiveness to this dietary intervention. Altogether, DR induces both memory T cells and the gut microbiota to produce essential, distinct factors that converge on myeloid cells to promote optimal pathogen control. These findings reveal how nutritional cues promote adaptation and co-operation between multiple immune cells and the gut microbiota, which synergize to optimize immunity and protect the collective metaorganism.
2023-12-13 | GSE242696 | GEO