Ontology highlight
ABSTRACT:
PROVIDER: PRJNA909964 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22573100_1.fastq.gz | Fastqsanger.gz | |||
| SRR22573100_2.fastq.gz | Fastqsanger.gz | |||
| SRR22573101_1.fastq.gz | Fastqsanger.gz | |||
| SRR22573101_2.fastq.gz | Fastqsanger.gz | |||
| SRR22573102_1.fastq.gz | Fastqsanger.gz |
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Project description:Fatty liver disease is prevalent during parturition in dairy cattle. Therefore, there is an urgent need to develop novel, sensitive biomarkers for the early diagnosis of the metabolic disorders. Macroproteomics revealed that the fecal microbial community changes significantly when animal develops fatty liver disease. The microbial changes in cows with severe fatty liver (SFL) were greater than cows with moderate fatty liver (MFL) and normal condition (Norm). This suggests that microorganisms play an important role in the pathogenesis of metabolic disorders. In this study, feces-sourced microorganisms and microbial proteins were identified and testified as novel biomarkers for the early diagnosis of fatty liver disease in cattle. For example, the AUC (area under curve) values, based on Receiver Operating Characteristics analysis, of using the combination of Lachnoanaerobaculum and Bifidobacterium (at the genus level) to discriminate MFL and SFL animals reached 0.944 and 0.867, respectively. and 0.922 and 0.985, respectively, for the combination of Bifidobacterium pseudolongum and Lachnospiraceae bacterium (at the species level). Interestingly, the differentially expressed microbial proteins are closely related to the identified microorganisms. For example, the majority of the top 20 microbial proteins with significant expression differences were derived from Bifidobacterium pseudolongum. Bifidobacterium pseudolongum was considered a prominent potential biomarker for the diagnosis of metabolic disorders, especially in fatty liver cattle. The results of this study confirm that microbial signatures have a causal contribution to the pathophysiological mechanism of non-alcoholic fatty liver disease (NAFLD), but also shed light on fecal microbiota transfer (FMT) experiments in treating NAFLD.
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Project description:Investigation of microbial community composition in mouse models using an intestinal epithial-specific and inducible VilCreERT2-mediated conditional knockout of Jup under basal conditions and in acute dextran-sodium sulfate (DSS)-induced colitis We investigated the gut microbiome composition in a dextran sulfate sodium (DSS) colitis model using Jupfl/fl and iVilCreERT2Jupfl/fl mice. Fecal samples were collected after DSS treatment, and 16S rRNA sequencing was employed to analyze microbial communities. Our findings revealed no significant differences in microbial profiles between Jupfl/fl and iVilCreERT2Jupfl/fl under DSS treatment.
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Project description:Morphine causes microbial dysbiosis. In this study we focused on restoration of native microbiota in morphine treated mice and looked at the extent of restoration and immunological consequences of this restoration. Fecal transplant has been successfully used clinically, especially for treating C. difficile infection2528. With our expanding knowledge of the central role of microbiome in maintenance of host immune homeostasis17, fecal transplant is gaining importance as a therapy for indications resulting from microbial dysbiosis. There is a major difference between fecal transplant being used for the treatment of C. difficile infection and the conditions described in our studies. The former strategy is based on the argument that microbial dysbiosis caused by disproportionate overgrowth of a pathobiont can be out-competed by re-introducing the missing flora by way of a normal microbiome transplant. This strategy is independent of host factors and systemic effects on the microbial composition. Here, we show that microbial dysbiosis caused due to morphine can be reversed by transplantation of microbiota from the placebo-treated animals.
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Project description:Opioids such as morphine have many beneficial properties as analgesics, however, opioids may induce multiple adverse gastrointestinal symptoms. We have recently demonstrated that morphine treatment results in significant disruption in gut barrier function leading to increased translocation of gut commensal bacteria. However, it is unclear how opioids modulate the gut homeostasis. By using a mouse model of morphine treatment, we studied effects of morphine treatment on gut microbiome. We characterized phylogenetic profiles of gut microbes, and found a significant shift in the gut microbiome and increase of pathogenic bacteria following morphine treatment when compared to placebo. In the present study, wild type mice (C57BL/6J) were implanted with placebo, morphine pellets subcutaneously. Fecal matter were taken for bacterial 16s rDNA sequencing analysis at day 3 post treatment. A scatter plot based on an unweighted UniFrac distance matrics obtained from the sequences at OTU level with 97% similarity showed a distinct clustering of the community composition between the morphine and placebo treated groups. By using the chao1 index to evaluate alpha diversity (that is diversity within a group) and using unweighted UniFrac distance to evaluate beta diversity (that is diversity between groups, comparing microbial community based on compositional structures), we found that morphine treatment results in a significant decrease in alpha diversity and shift in fecal microbiome at day 3 post treatment compared to placebo treatment. Taxonomical analysis showed that morphine treatment results in a significant increase of potential pathogenic bacteria. Our study shed light on effects of morphine on the gut microbiome, and its role in the gut homeostasis.
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Project description:In this study, samples of 16 dairy cows from a MAP infected farm were used. Serum, milk and fecal samples were collected. Categorizing these cows into two groups based on their MAP infection status different standard methods for detection MAP were applied. Healthy controls showed no positive results in enzyme-linked immunosorbent assay (ELISA) with serum and milk samples (cattletype MAP Ab, Qiagen, Hilden, Germany; In-direct, IDVet, Grabels, France) and after cultivation of fecal samples on commercial Her-rold´s Egg Yolk Agars (HEYM agar, Becton Dickinson, Heidelberg, Germany) for 12 weeks. Cows with positive results were grouped into MAP infected cows. Specifically, for mass spectrometry analysis serum of seven MAP infected cows and seven healthy controls were used. All animals were from the same farm and were kept under the same environmental conditions. For additional mass spectrometry analysis with a further control group sam-ples of 21 dairy cows from an uninfected farm were examined. All cattle from this farm showed negative results in ELISA with serum and milk samples. Additionally, there was never a positive result in regularly tested fecal samples and sock swab samples of this farm. For verification of differential CTSS expression in Western blot analysis five dairy cows from another infected farm were consultedincluded. MAP status of these cows was analyzed by cultivation of fecal samples on HEYM agar for 12 weeks and ELISA with se-rum samples. In detail, two cattle were categorized into healthy controls and three cattle into MAP infected cows. Withdrawal of bovine venous whole blood and experi-mental protocols were approved by the local authority, Government of Upper Bavaria, permit no. ROB-55.2-2532.Vet_03-17-106.
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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).
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Project description:<p>Left displaced abomasum (LDA) in postpartum dairy cows contributes to significant economic losses. LDA is characterized by excessive lipolysis and insulin resistance. Although gut dysbiosis is implicated, little is known about the role of the gut microbiota in the abnormal metabolic processes of LDA. To investigate the functional links among microbiota, metabolites, and disease phenotypes in LDA, we performed liquid chromatography-tandem mass spectrometry of fecal samples from cows with LDA (n = 10) and healthy cows (n = 10) matched for parity and days in milk. Plasma marker profiling was synchronously analyzed. Compared with the healthy group, the LDA group showed increased alpha diversity and a shifted microbial community, accompanied by differences in the fecal metabolome and plasma amino acid pools. Based on integrated analysis with the plasma metabolome, eight genera and eight metabolites were associated with LDA. Akkermansia and Oscillospira abundances negatively correlated with 4-pyridoxic acid and tryptophan levels, and positively correlated with non-esterified fatty acid (NEFA) and β-hydroxybutyric acid (BHBA) in amino acid deficit, indicating pyridoxal metabolism-associated gut dysbiosis and lipolysis. The level of salicylic acid derived from microbiota catabolism was decreased in LDA, which negatively correlated with Prevotella, NEFA, and BHBA levels. Conversely, levels of lithocholic acid and taurolithocholic acid were increased in cows with LDA. Changes in branched-chain amino acids implicated novel host–microbial metabolic pathways involving lipolysis and insulin resistance in cows with LDA. Overall, these results suggest interplay between host and gut microbes contributing to LDA pathogenesis.</p>
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