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ABSTRACT:
PROVIDER: PRJNA810285 | ENA |
REPOSITORIES: ENA
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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: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 purpose of this study was to interrogate the role of EGF-family ligands, in particular Epidermal Growth Factor (EGF) and Neuregulin 1 (NRG1), as human intestinal stem cell niche factors. An established duodenal enteroid line derived from a 20.2 week post conception biological specimen was exposed to either EGF or NRG1 for five days, after which scRNA-seq was performed to assess changes in gene expression and cellular composition. In an independent experiment, scRNA-seq was performed on freshly isolated duodenal epithelium from a 15 week specimen cultured in the presence of EGF, NRG1, or both EGF and NRG1 after 2 passages.
2020-12-10 | E-MTAB-9720 | biostudies-arrayexpress
Project description:The aim of this study is to characterise and compare the composition of the microbiota from sputum samples of cystic fibrosis sufferers from different centres. These data are part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
2014-09-16 | E-ERAD-265 | biostudies-arrayexpress
Project description:This study aimed to analyze changes in gut microbiota composition in mice after transplantation of fecal microbiota (FMT, N = 6) from the feces of NSCLC patients by analyzing fecal content using 16S rRNA sequencing, 10 days after transplantation. Specific-pathogen-free (SPF) mice were used for each experiments (N=4) as controls.
2023-07-01 | E-MTAB-12812 | biostudies-arrayexpress
Project description:Tissue lymphatics are crucial for fluid homeostasis and immunosurveillance. We asked whether the lymphatics are adapted to the organ in which they reside, such as along the gut. Duodenal lymphatic capillaries (lacteals) displayed the mot discontinuous tight junction composition versus lacteals at other sites, resulting in a dependence on duodenal lacteals for rapid dietary lipid uptake. Duodenal helminths abrogated these features. RNAseq of LECs and the mucosa along the intestine revealed that LEC transcriptomes matched the functional profile of the local mucosa. Helminth infection reverses key duodenal signatures like lipid metabolism and immune activation, instead triggering lymphangiogenic and mucosal antimicrobial responses. We identified a putative VEGFR2/3 signaling gradient that may explain differences in tight junction along the small intestine at homeostasis. Inflammation-induced lymphangiogenesis and decreased fat exposure likely underlie duodenal lymphatic impermeability upon helminth infection, while microbial depletion acted additively on lymphatic restructuring. Our study provides molecular insights into lymphatic function along the intestine and stages lymphatic permeability as subject to dynamic regulation by environmental queues.
2024-07-08 | GSE271712 | GEO
Project description:Tissue lymphatics are crucial for fluid homeostasis and immunosurveillance. We asked whether the lymphatics are adapted to the organ in which they reside, such as along the gut. Duodenal lymphatic capillaries (lacteals) displayed the mot discontinuous tight junction composition versus lacteals at other sites, resulting in a dependence on duodenal lacteals for rapid dietary lipid uptake. Duodenal helminths abrogated these features. RNAseq of LECs and the mucosa along the intestine revealed that LEC transcriptomes matched the functional profile of the local mucosa. Helminth infection reverses key duodenal signatures like lipid metabolism and immune activation, instead triggering lymphangiogenic and mucosal antimicrobial responses. We identified a putative VEGFR2/3 signaling gradient that may explain differences in tight junction along the small intestine at homeostasis. Inflammation-induced lymphangiogenesis and decreased fat exposure likely underlie duodenal lymphatic impermeability upon helminth infection, while microbial depletion acted additively on lymphatic restructuring. Our study provides molecular insights into lymphatic function along the intestine and stages lymphatic permeability as subject to dynamic regulation by environmental queues.
2024-07-08 | GSE271711 | GEO