Ontology highlight
ABSTRACT:
PROVIDER: PRJNA707106 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13891627_1.fastq.gz | Fastqsanger.gz | |||
| SRR13891627_2.fastq.gz | Fastqsanger.gz | |||
| SRR13891628_1.fastq.gz | Fastqsanger.gz | |||
| SRR13891628_2.fastq.gz | Fastqsanger.gz | |||
| SRR13891629_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 80 |
Similar Datasets
Project description:Obesity is associated with an increased risk of mucosal infections; however, the mechanistic basis of this phenomenon remains incompletely defined. Intestinal mucus barrier systems normally prevent infections, but are sensitive to changes in the luminal environment. Here we demonstrate that mice exposed to an obesogenic Western-style diet (WSD) suffer regiospecific failure of the mucus barrier in the small intestinal jejunum caused by diet-induced mucus condensation, which occurs independently of microbiota alterations. Mucus barrier disruption due to either WSD exposure or chromosomal Muc2 deletion results in collapse of the commensal jejunal microbiota, which in turn sensitises mice to atypical jejunal colonization by the enteric pathogen Citrobacter rodentium. We identify the jejunal mucus layer as a microbial habitat, and link the regiospecific mucus dependency of the microbiota to fundamental properties of the jejunal niche. Together, our data identifies a symbiotic mucus-microbiota relationship that normally prevents jejunal pathogen colonization, but is highly sensitive to disruption by exposure to a Western-style diet.
2023-05-12 | PXD028613 | Pride
Project description:Alterations in intestinal microbiota and intestinal short chain fatty acids profiles have been associated with the pathophysiology of obesity and insulin resistance. Whether intestinal microbiota dysbiosis is a causative factor in humans remains to be clarified We examined the effect of fecal microbial infusion from lean donors on the intestinal microbiota composition, glucose metabolism and small intestinal gene expression. Male subjects with metabolic syndrome underwent bowel lavage and were randomised to allogenic (from male lean donors with BMI<23 kg/m2, n=9) or autologous (reinfusion of own feces, n=9) fecal microbial transplant. Insulin sensitivity and fecal short chain fatty acid harvest were measured at baseline and 6 weeks after infusion. Intestinal microbiota composition was determined in fecal samples and jejunal mucosal biopsies were also analyzed for the host transcriptional response. Insulin sensitivity significantly improved six weeks after allogenic fecal microbial infusion (median Rd: from 26.2 to 45.3 μmol/kg.min, p<0.05). Allogenic fecal microbial infusion increased the overall amount of intestinal butyrate producing microbiota and enhanced fecal harvest of butyrate. Moreover, the transcriptome analysis of jejunal mucosal samples revealed an increased expression of genes involved in a G-protein receptor signalling cascade and subsequently in glucose homeostasis. Lean donor microbial infusion improves insulin sensitivity and levels of butyrate-producing and other intestinal microbiota in subjects with the metabolic syndrome. We propose a model wherein these bacteria provide an attractive therapeutic target for insulin resistance in humans. (Netherlands Trial Register NTR1776).
2020-10-28 | GSE30854 | GEO
Project description:An early settlement of a complex gut microbiota can protect against gastro-intestinal dysbiosis, but the effects of neonatal microbiota colonization on the gut barrier upon the further encounter of favorable bacteria or not, are largely unknown. The jejunal transcriptome of differently perfused intestinal loops of 12 caesarian-derived pigs previously associated with microbiota of different complexity was studied. Pigs received pasteurized sow colostrum at birth (d0), 2 mL of starter microbiota (10^7 CFU of each Lactob. Amylovorus (LAM), Clostr. glycolicum, and Parabacteroides spp.) on d1-d3 of age and either a placebo inoculant (simple association, SA) or an inoculant consisting of diluted feces of an adult sow (complex association, CA) on d3-d4 of age. On days 26-37 of age, jejunal loops were perfused for 8 h with either enterotoxigenic E. coli F4 (ETEC), F4 fimbriae (F4), LAM or saline (CTRL) and jejunal samples were obtained from each piglet immediately afterwards. The analysis of whole mRNA transcript expression was done by Affymetrix©Porcine Gene 1.1 ST array strips, a Robust Multichip Analysis was performed on the CEL files, and Transcripts IDâs were associated to 13,406 Human gene names, based on Sus scrofa Ensemble
2016-02-11 | E-GEOD-77787 | biostudies-arrayexpress
Project description:An experiment was conducted to investigate the effects of dietary inclusion of rye, a model ingredient to increase gut viscosity, between 14 and 28 days of age on immune competence related parameters and performance of broiler. A total number of 960 one-day-old male Ross 308 chicks were weighed and randomly allocated to 24 pens (40 birds per pen), and the birds in every 8 replicate pens were assigned to one of three experimental diets including graded levels, 0%, 5%, and 10% of rye. Tested immune competence related parameters were composition of the intestinal microbiota, genes expression in gut tissue, and gut morphology. The inclusion of 5% or 10% rye in the diet (d14-28) resulted in decreased performance and litter quality, but in increased villus height and crypt depth in the small intestine (jejunum) of the broilers. Relative bursa and spleen weights were not affected by dietary inclusion of rye. In the jejunum, no effects on number and size of goblet cells, and only trends on microbiota composition in the digesta were observed. Dietary inclusion of rye affected expression of genes involved in cell cycle processes of the jejunal enterocyte cells, thereby influencing cell growth, cell differentiation and cell survival, which in turn were consistent with the observed differences in the morphology of the gut wall. In addition, providing rye-rich diets to broilers affected the complement and coagulation pathways, which are parts of the innate immune system. These pathways are involved in eradicating invasive pathogens. Overall, it can be concluded that inclusion of 5% or 10% rye to the grower diet of broilers had limited effects on performance. Ileal gut morphology, microbiota composition of jejunal digesta, and gene expression profiles of jejunal tissue, however, were affected by dietary rye inclusion level, indicating that rye supplementation to broiler diets might affect immune competence of the birds.
2017-04-19 | GSE94095 | GEO
Project description:We profiled transcriptome and chromatin landscapes in jejunal mouse intestinal epithelial cells (IECs) from mice reared in the absence (Germ Free or GF) or presence (Conventionalized or CV) of microbiota. We show that microbiota colonization results in changes in histone modifications at hundreds of enhancers that are associated with microbiota-regulated genes. Furthermore, we show that microbiota colonization is associated with a drastic genome-wide reduction in Hnf4a and Hnf4g binding.
2017-03-27 | GSE90461 | GEO
Project description:An early settlement of a complex gut microbiota can protect against gastro-intestinal dysbiosis, but the effects of neonatal microbiota colonization on the gut barrier upon the further encounter of favorable bacteria or not, are largely unknown. The jejunal transcriptome of differently perfused intestinal loops of 12 caesarian-derived pigs previously associated with microbiota of different complexity was studied. Pigs received pasteurized sow colostrum at birth (d0), 2 mL of starter microbiota (10^7 CFU of each Lactob. Amylovorus (LAM), Clostr. glycolicum, and Parabacteroides spp.) on d1-d3 of age and either a placebo inoculant (simple association, SA) or an inoculant consisting of diluted feces of an adult sow (complex association, CA) on d3-d4 of age. On days 26-37 of age, jejunal loops were perfused for 8 h with either enterotoxigenic E. coli F4 (ETEC), F4 fimbriae (F4), LAM or saline (CTRL) and jejunal samples were obtained from each piglet immediately afterwards.
2016-02-11 | GSE77787 | GEO
Project description:<p>Although nonstarch polysaccharides often have growth-promoting effects in animals, little is known about how polysaccharides act when administered as feed additives. Here, we demonstrate that Amomum longiligulare polysaccharide 1 (ALP1) improves the growth performance of piglets by promoting the proliferation of jejunal epithelial cells. ALP1 can be absorbed by jejunal epithelial cells via endocytosis and increases the ratio of cells in the S and G2/M phases by increasing the expression of CDK4 and Cyclin E, which increases the number of proliferating cells. The gut microbiota is an important regulatory target of polysaccharides. ALP1 supplementation can increase the abundance of Lactobacillus in the jejuna of piglets, resulting in a high abundance of 11Z-eicosenoic acid (EA). In addition, EA increases the villus length in the jejunum by promoting cell proliferation. Our findings indicate that oral ALP1 supplementation promotes growth by direct (acting on jejunal epithelial cells) and indirect (acting on jejunal microbiota) mechanisms.</p>
2024-08-01 | MTBLS9835 | MetaboLights
Project description:Emerging knowledge shows the importance of early life events in programming the intestinal mucosal immune system and development of the intestinal barrier function. These processes depend heavily on close interactions between gut microbiota and host cells in the intestinal mucosa. In turn, development of the intestinal microbiota is largely dependent on available nutrients and substrates required for the specific microbial community structures to expand. It is currently not known what the specificities are of intestinal microbial community structures in relation to the programming of the intestinal mucosal immune system and development of the intestinal barrier function. The objective of the present study was to investigate the effect of a nutritional intervention on intestinal development of suckling piglets by daily oral administration of fructooligosaccharides (FOS) over a period of 12 days. At the microbiota community level a clear “bifidogenic” effect of the FOS administration was observed in colon digesta at day 14. The former, however, did not translate into significant changes of local gene expression in the colonic mucosa. In the jejunum, significant changes were observed for microbiota composition at day 14, and microbiota diversity at day 25. In addition, significant differentially expressed gene sets in mucosal tissues of jejunum were identified at both days 14 and 25 of age. At the age of 14 days, lower activity of cell cycle-related processes and a higher activity of extracellular matrix processes were observed in jejunal scrapings of piglets supplemented with FOS compared to control piglets. At day 25, lower activity of immune-related processes in jejunal tissue were seen in piglets supplemented with FOS. Histological parameters, villi height and crypt depth, were significantly different at day 25 between the experimental and control group, where piglets supplemented with FOS had higher villi and deeper crypts. We conclude that oral FOS administration during the suckling period of piglets has significant bifidogenic effects on the microbiota in the colon and on gene expression in jejunal mucosa scrapings. We hypothesize that FOS supplementation of suckling piglets results in a higher butyrate production in the colon due to the increase in bifidobacteria and lactobacilli in the hindgut. We further speculate that a higher butyrate production in colonic digesta relates to changes in gene expression in the jejunum by thus far unknown mechanisms.
2018-01-29 | GSE101147 | GEO
Project description:The potential of orally administered colostrum-derived EVs to regulate gut microbiota dysbiosis and prevent non-alcoholic steatohepatitis was evaluated. The results demonstrated that colostrum-derived EVs improved steatosis, fibrosis, and inflammation. Transcriptome analysis showed decreased lipid metabolism, bacterial response, and inflammatory responses in the intestine, and reduced inflammatory and fibrosis-related pathways in the liver. Gut microbiota and metabolite analysis revealed an increased abundance of Akkermansia and elevated cholesterol excretion. Additionally, treatment with colostrum-derived EVs increased the production of tight junction proteins and mucin in the intestine. These findings suggest that increased Akkermansia due to colostrum-derived EVs improves intestinal inflammation and barrier function, preventing endotoxin translocation to the liver and thereby reducing liver inflammation and fibrosis.
2024-08-01 | GSE273582 | GEO