Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1173338 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31054644_1.fastq.gz | Fastqsanger.gz | |||
| SRR31054644_2.fastq.gz | Fastqsanger.gz | |||
| SRR31054645_1.fastq.gz | Fastqsanger.gz | |||
| SRR31054645_2.fastq.gz | Fastqsanger.gz | |||
| SRR31054646_1.fastq.gz | Fastqsanger.gz |
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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:The aim of this study was to explore whether, and if so, how Bacillus subtilis KC1 can enhance the growth performance of broilers that have been adversely affected by Mycoplasma gallisepticum (MG) infection. A total of 96 1-day-old male broilers were randomly divided into 4 groups: the control group (basal diet), the MG group (basal diet + MG challenge), the Bacillus subtilis KC1 group (basal diet + Bacillus subtilis KC1 supplementation), the Bacillus subtilis KC1 + MG group (basal diet + Bacillus subtilis KC1 supplementation + MG challenge). The trial lasted 42 days, and the results showed that the MG group had significantly reduced body weight and average daily gain, as well as increased feed conversion ratio of broilers, compared to the control group. Dietary supplementation with Bacillus subtilis KC1 significantly improved the growth performance of MG-infected broilers. In addition, dietary supplementation with Bacillus subtilis KC1 significantly improved oxidative stress and inflammatory response markers, characterized by increased superoxide dismutase levels and reduced levels of malondialdehyde, interleukin-1β, and tumor necrosis factor-α. Furthermore, both metabolomics and transcriptomics analyses indicated that MG infection markedly disrupted amino acid metabolism in broilers, whereas Bacillus subtilis KC1 supplementation alleviated the abnormal amino acid metabolism caused by MG infection. These results suggested that Bacillus subtilis KC1 may alleviate the poor growth performance caused by MG infection in broilers by improving amino acid metabolism.
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Project description:The objectives of this study were to determine the protective effects of organic acids (OA) in broilers exposed to Salmonella Pullorum challenge at early stage and to explore the potential benefits of OA by metabolomics analysis. The treatment groups included non-challenged, S. Pullorum-challenged, challenged group supplemented with virginiamycin, challenged group supplemented with OA in drinking water, challenged group supplemented with OA in feed, and challenged group supplemented with OA in combination in drinking water and feed. Results showed that early Salmonella challenge induced an acute systemic infection of broilers in the starter phase, followed by the grower phase without triggering clinical signs. OA supplementation promoted growth during the grower phase, and while OA in water contributed more, the positive effects of OA in combination were comparable to those of virginiamycin supplementation in challenged birds. Furthermore, OA could modulate the systemic metabolic perturbation caused by challenge as it alleviated stress responses mediated by steroid hormone, potentially attenuated antioxidant or immune defense, and modified intestinal microbiota metabolism. These results show a metabolic mechanism that may partly explain the potential benefits of OA in Salmonella challenged birds, and may contribute to the use of OA to control or reduce S. Pullorum infection in farm animals.
2021-05-17 | MTBLS1274 | MetaboLights
Project description:Background: The long-term high-fat, high-sugar diet exacerbates type 2 diabetes mellitus (T2DM)-related cognitive impairments. The negative impact of poor dietary patterns on brain development and neurological function may be related to gut microbiota disturbance. The role of phlorizin in mitigating glucose and lipid metabolism disorders is well documented. However, the protective effect of phlorizin on diabetes-related cognitive dysfunction is unclear. Therefore, the present study aimed to investigate the effect of dietary supplementation of phlorizin on high-fat and high-fructose diet (HFFD)-induced cognitive dysfunction and evaluate the crucial role of the microbiota-gut-brain axis. Results: Dietary supplementation of phlorizin for 14 weeks effectively prevented glucolipid metabolism disorder, spatial learning impairment, and memory impairment in HFFD mice. In addition, phlorizin improved the HFFD-induced decrease in synaptic plasticity, neuroinflammation, and excessive activation of microglia in the hippocampus. Transcriptomics analysis shows that the protective effect of phlorizin on cognitive impairment was associated with increased expression of neurotransmitters and synapse-related genes in the hippocampus. Phlorizin treatment alleviated colon microbiota disturbance, mainly manifested by an increase in gut microbiota diversity and the abundance of short-chain fatty acid (SCFA)-producing bacteria. The level of microbial metabolites, including SCFA, inosine 5'-monophosphate (IMP), and D (-)-beta-hydroxybutyric acid (BHB) were also significantly increased after phlorizin treatment. Moreover, integrating multiomics analysis observed tight connections between phlorizin-regulated genes, microbiota, and metabolites. Furthermore, removal of the gut microbiota via antibiotics treatment diminished the protective effect of phlorizin against HFFD-induced cognitive impairment, underscoring the critical role of the gut microbiota in mediating cognitive behavior. Importantly, supplementation with SCFA and BHB alone mimicked the regulatory effects of phlorizin on cognitive function. Conclusions: These results indicate that gut microbiota and their metabolites mediate the ameliorative effect of phlorizin on HFFD-induced cognitive impairment. Therefore, phlorizin can be used as an easy-to-implement nutritional therapy to prevent and alleviate metabolism-related neurodegenerative diseases by targeting the regulation of the microbiome-gut-brain axis.
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Project description:The chicken gastrointestinal tract (GIT) harbours a complex microbial community, involved in several physiological processes such as host immunomodulation and feed digestion. Other studies were already performed to define the chicken gut metagenome and its fecal metaproteome. For the first time, the present study analysed dietary effects on the protein inventory of the microbiota in crop and ceca of broilers. We performed quantitative label-free metaproteomics by using 1D-gel electrophoresis coupled with LC-MS/MS to identify the structural and functional changes triggered by diets supplied with varying amount of mineral phosphorus (P) and microbial phytase (MP). Phylogenetic assessment based on label-free quantification (LFQ) values of the proteins identified Lactobacillaceae as the major family in the crop section regardless of the diet, whereas proteins belonging to the family Veillonellaceae increased with the P supplementation. Within the ceca section, proteins of Bacteroidaceae were more abundant in the P-supplied diets, whereas proteins of Eubacteriaceae decreased with the P-addition. Proteins of the Ruminococcaceae increasedraised with the amount of MP while proteins of Lactobacillaceae werewas more abundant in the MP-lacking diets. Classification of the identified proteins into COGs and KEGG pathways underlined a diverse microbiota activity depending on the dietary regimen, indicating a thriving microbial community in the case of P and MP supplementation, and stressed microbial community when no P and MP were supplied. Insights oninto the identified KEGG pathways, as well as comparison between the GIT sections, dietary treatments, and the bacterial families encoding for the pathways of interest are provided. T) harbours a complex microbial community, involved in several physiological processes such as host immunomodulation and feed digestion. Other studies were already performed to define the chicken gut metagenome and its fecal metaproteome. For the first time, the present study analysed dietary effects on the protein inventory of the microbiota in crop and ceca of broilers. We performed quantitative label-free metaproteomics by using 1D-gel electrophoresis coupled with LC-MS/MS to identify the structural and functional changes triggered by diets supplied with varying amount of mineral phosphorus (P) and microbial phytase (MP). Phylogenetic assessment based on label-free quantification (LFQ) values of the proteins identified Lactobacillaceae as the major family in the crop section regardless of the diet, whereas proteins belonging to the family Veillonellaceae increased with the P supplementation. Within the ceca section, proteins of Bacteroidaceae were more abundant in the P-supplied diets, whereas proteins of Eubacteriaceae decreased with the P-addition. Proteins of the Ruminococcaceae increasedraised with the amount of MP while proteins of Lactobacillaceae werewas more abundant in the MP-lacking diets. Classification of the identified proteins into COGs and KEGG pathways underlined a diverse microbiota activity depending on the dietary regimen, indicating a thriving microbial community in the case of P and MP supplementation, and stressed microbial community when no P and MP were supplied. Insights oninto the identified KEGG pathways, as well as comparison between the GIT sections, dietary treatments, and the bacterial families encoding for the pathways of interest are provided.
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Project description:Iron is an essential metal for both animals and microbiota, and neonates and infants of humans and animals, in general, are at the risk of iron insufficient. However, excess dietary iron usually causes negative impacts on the host and microbiota. This study aimed to investigate over-loaded dietary iron supplementation on growth performance, the distribution pattern of iron in the gut lumen and the host, intestinal microbiota, and intestine gene expression profile of piglets. Sixty healthy weaning piglets were randomly assigned to six groups: fed with diets supplemented with ferrous sulfate monohydrate at the dose of 50ppm (Fe50 group), 100ppm (Fe100 group), 200ppm (Fe200 group), 500ppm (Fe500 group), and 800ppm (Fe800) for three weeks. The results indicated that increasing iron had no effects on growth performance but increased diarrheal risk and iron deposition in intestinal digesta, tissues of intestine and liver, and serum. High iron also reduced serum iron-binding capacity, apolipoprotein, and immunoglobin A. The RNA-sequencing analysis revealed that iron changed colonic gene expression profile, such as interferon gamma-signal transducer and activator of transcription 2 based anti-virus and bacteria gene network. Increasing iron also shifted cecal and colonic microbiota, such as reducing alpha diversity, Clostridiales and Lactobacillus reuteri, and increasing Lactobacillus and Lactobacillus amylovorus. Collectively, this study demonstrated that high dietary iron increased diarrheal incidence, changed intestinal immune response-associated gene expression, and shifts gut microbiota. The results would enhance our knowledge of iron effects on the gut and microbiome in piglets, and further contribute to understanding these aspects in humans.
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Project description:The molecular mechanisms by which dietary fruits and vegetables confer cardiometabolic benefits remain poorly understood. Historically, these beneficial properties have been attributed to the antioxidant activity of flavonoids. Here, we reveal that the host metabolic benefits associated with flavonoid consumption actually hinge on gut microbial metabolism. However, flavonoids are consumed in a largely glycosylated form, rendering them poorly available for small intestinal absorption and subjecting them to microbial metabolism in the colon. We show that a single gut microbial flavonoid catabolite is sufficient to reduce diet-induced cardiometabolic disease burden in mice. Dietary supplementation with elderberry extract attenuated obesity and continuous delivery of the catabolite 4-hydroxphenylacetic acid was sufficient to reverse hepatic steatosis. Analysis of human gut metagenomes revealed that under one percent contains a flavonol catabolic pathway, underscoring the rarity of this process. Our study will impact the design of dietary and probiotic interventions to complement traditional cardiometabolic treatment strategies.
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Project description:Intestinal Foxp3+ regulatory T cell (Treg) subsets are crucial players in tolerance to microbiota-derived and food-borne antigens, and compelling evidence suggests that the intestinal microbiota modulates their generation, functional specialization, and maintenance. Selected bacterial species and microbiota-derived metabolites, such as short-chain fatty acids (SCFAs), have been reported to promote Treg homeostasis in the intestinal lamina propria. Furthermore, gut-draining mesenteric lymph nodes (mLNs) are particularly efficient sites for the generation of peripherally induced Tregs (pTregs). Despite this knowledge, the direct role of the microbiota and their metabolites in the early stages of pTreg induction within mLNs is not fully elucidated. Here, using an adoptive transfer-based pTreg induction system, we demonstrate that neither transfer of a dysbiotic microbiota nor dietary SCFA supplementation modulated the pTreg induction capacity of mLNs. Even mice housed under germ-free (GF) conditions displayed equivalent pTreg induction within mLNs. Further molecular characterization of these de novo induced pTregs from mLNs by dissection of their transcriptomes and accessible chromatin regions revealed that the microbiota indeed has a limited impact and does not contribute to the initialization of the Treg-specific epigenetic landscape. Overall, our data suggest that the microbiota is dispensable for the early stages of pTreg induction within mLNs.
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