Ontology highlight
ABSTRACT:
PROVIDER: PRJNA914498 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22839329_1.fastq.gz | Fastqsanger.gz | |||
| SRR22839329_2.fastq.gz | Fastqsanger.gz | |||
| SRR22839330_1.fastq.gz | Fastqsanger.gz | |||
| SRR22839330_2.fastq.gz | Fastqsanger.gz | |||
| SRR22839331_1.fastq.gz | Fastqsanger.gz |
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Project description:Undernutrition disrupts cecal microbiota and epithelium interactions and epithelial metabolism and immune response in a pregnant sheep model
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Project description:Transcriptomics and functional bioinformatics were used to investigate the potential interactions of undernutrition and the presence of the conceptus at the time of maternal recognition of pregnancy on uterine indicators of metabolism and reproduction. Adult Rasa Aragonesa ewes were allocated to one of two planes of nutrition during 28 days: maintenance energy intake (control; 5 cyclic, 6 pregnant ewes) providing 7.8 MJ of metabolisable energy per ewe and 0.5 maintenance intake (undernourished; 6 cyclic, 7 pregnant ewes) providing 3.9 MJ of metabolisable energy per ewe. RNA from uterine tissue was harvested at slaughter on day 14 of estrus or pregnancy, and hybridized to the Agilent 15K Sheep Microarray chip. Functional bioinformatics analyses were performed using the Dynamic Impact Approach (DIA) and Ingenuity Pathway Analysis. Among metabolic pathways, citrate cycle, oxidative phosphorylation, pentose and glucuronate interconversions and biosynthesis of unsaturated fatty acids were upregulated in control pregnant compared with control cyclic ewes. However, these pathways were not altered in undernourished ewes. The presence of an embryo in undernourished ewes upregulated fatty acid and glycogenic amino acid metabolism. RIG-I and Toll like receptors and chemokine signaling pathways were upregulated by the presence of the embryo in both control and undernourished ewes, but in the latter group the impact was lower. Undernutrition alone upregulated carbohydrate metabolism, but different pathways were altered in cyclic versus pregnant ewes. Citrate cycle, glycolysis/gluconeogenesis, and pentose and glucuronate interconversions were upregulated in undernourished cyclic compared with control cyclic ewes. Glycolysis/gluconeogenesis, pyruvate and propanoate metabolism, beta-alanine and phenylalanine metabolism were upregulated in undernourished pregnant compared with control pregnant ewes, whereas biosynthesis of unsaturated fatty acids and replication and repair were downregulated. Undernutrition alone led to an overall weak activation of immune system pathways both in cyclic and pregnant ewes. However, undernourished cyclic compared with control cyclic ewes had a high activation of NOD-like and RIG-1 like receptor signaling pathways, whereas undernourished pregnant compared with control pregnant ewes only had a weak upregulation of T cell receptor signaling pathways. Overall, data revealed that metabolic and immune adaptations of the uterus to nutrient restriction are dependent on the presence of the conceptus.
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Project description:Undernutrition disrupts jejunal and ileal microbiota and epithelial tissue homeostasis in a pregnant sheep model
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Project description:There is much evidence suggesting that gene-environment interactions underlying the developmental origins of the metabolic syndrome. Previously, we have induced a metabolic syndrome phenotype in mice though prenatal undernutrition; however, the C57BL/6J strain exhibited significantly more metrics of the metabolic syndrome than the A/J strain. We used microarrays to detail the global programme of gene expression underlying the strain differences in the prenatal induction of the adult development of the metabolic syndrome. We focused on liver function and gene expression because of it's centrol role in many aspects of the metabolic syndrome including glucose and lipid control. Keywords: disease state analysis between mouse strains Pregnant A/J and C57BL/6J mice were either exposed to prenatal undernutrition during pregnancy or control conditions. The livers from 32 male offspring (8 per group within each of the two strains) were dissected out at 7 months of age and total RNA was extracted and hybridization on Affymetrix microarrays.
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Project description:We have identified statistically significant SNPs influencing susceptibility to diarrhea due to Entamoeba histolytica infection at the locus encoding the transcription factor CREM (10p11.21; rs58000832, P=6.1x10-9; rs2148483, P=9.6x10-8) using genome wide association studies (GWAS). Considering undernutrition increases susceptibility to enteric infection, we investigated if CREM locus variants were also associated with nutritional status. Genetic analysis on birth cohorts of Bangladeshi children demonstrated that risk alleles of rs58000832 and rs2148483 were associated with lower weight-for-age z-scores at 12 months of age (rs2148483: 0.188 reduction in WAZ, P= 0.014; rs58000832: 0.135 reduction in WAZ, P= 0.001), independent of E. histolytica diarrhea. Small intestinal transcriptome data from children homozygous for the rs2148483 risk allele compared to heterozygotes demonstrated enrichment of mitochondrial function and catabolism among upregulated genes and enrichment of B-cell activation and adaptive immune pathways among downregulated genes, consistent with dual roles of the CREM locus in immunity and metabolism. Full body deletion and/or intestinal epithelial cell (IEC)-specific deletion of CREM in mice produced decreased body weight. Transcriptome analysis of cecal tissue from E. histolytica challenged mice also showed upregulation of metabolic processes in both full body and IEC-specific deletion mice. Processes with downregulated genes in full body deletion mice were enriched for myeloid cell activation and chemotaxis while immune process changes were absent when deletion was limited to IECs. These data suggest that CREM modulates both metabolism and immune function at mucosal sites.
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Project description:When transmitted through the oral route, Toxoplasma gondii first interacts with its host at the small intestinal epithelium. This interaction is crucial to controlling initial invasion and replication, as well as shaping the quality of the systemic immune response. It is therefore an attractive target for the design of novel vaccines and adjuvants. However, due to a lack of tractable infection models, we understand surprisingly little about the molecular pathways that govern this interaction. The in vitro culture of small intestinal epithelium as host-pathogen intreaction shows great promise for modelling the epithelial response to infection. However, the enclosed luminal space makes the application of infectious agents to the apical epithelial surface challenging. Here, we have developed three novel enteroid-based techniques for modelling T. gondii infection. In particular, we have adapted enteroid culture protocols to generate collagen-supported epithelial sheets with an exposed apical surface. These cultures retain epithelial polarization, and the presence of fully differentiated epithelial cell populations. They are susceptible to infection with, and support replication of, T. gondii. Using quantitative label-free mass spectrometry, we show that T. gondii infection of the enteroid epithelium is associated with up-regulation of proteins associated with cholesterol metabolism, extracellular exosomes, intermicrovillar adhesion, and cell junctions. Inhibition of host cholesterol and isoprenoid biosynthesis with Atorvastatin resulted in a dramatic reduction in parasite replication. These novel models therefore offer tractable tools for investigating how interactions between T. gondii and the host intestinal epithelium influence the course of infection.
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Project description:Ruminant livestock are one of the major contributors to carbon emission contributing the global warming issue. Methane (CH4) produced from enteric microbial fermentation of feed in the reticulo-rumen are known to differ between sheep with different digestive function and fermentation products such as metabolites. However, the molecular mechanism underpinning differences in methane emission remains to be fully elucidated. We extracted a membrane and cytosolic protein fraction of rumen epithelium proteins from both high (H) and low (L) CH4 emitting sheep. Protein abundance differences between the phenotypes were quantified using SWATH-mass spectrometry. We identified 92 proteins annotated as cell surface transporters, of which only solute carrier family (SLC) 40A1 had a greater fold change of protein expression in the high methane emission phenotype. The main difference in protein abundance we found were related to the metabolism of glucose, lactate and processes of cell defence against microbes in the epithelium of sheep in each group. To best of our knowledge, this represents one of the most comprehensive proteomes of ovine rumen epithelium to date.
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