Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1033905 | ENA |
REPOSITORIES: ENA
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Project description:Nutritional supplementation is emerging as a promising strategy to support the clinical management of early Alzheimer’s disease (AD), partly through modulation of the intestinal microbiome via the microbiota–gut–brain axis. This study investigated the impact of Fortasyn Connect (Souvenaid®), a multinutrient formulation, on the gut microbiota using a dual approach: i) a dynamic gastrointestinal simulator (simgi®) inoculated with fecal samples from AD patients, and ii) an observational study involving early-stage AD patients (n = 22) receiving or not the supplement. The in vitro model provided a host-independent assessment of microbiota responses, revealing increased Bifidobacterium and Lactobacillus levels, along with enhanced short-chain fatty acid (SCFA) production. In patients, supplementation was associated with higher fecal abundance of Bifidobacterium and Christensenellaceae, reduced inflammatory markers (calprotectin and myeloperoxidase), and elevated butyrate levels. Fecal lipidomic and proteomic analyses indicated improved lipid digestion, increased secretory IgA, and modulation of host proteins related to gut–brain homeostasis. Systemically, higher circulating levels of iron, folate, and vitamin B12 were also observed. This study demonstrates that multinutrient supplementation such as Fortasyn Connect can beneficially modulate the gut ecosystem and immune–metabolic pathways in early AD, targeting disease-relevant mechanisms through the gut–brain axis in the context of aging.
2025-12-03 | PXD069669 | Pride
Project description:A human gut-on-a-chip microdevice was used to coculture multiple commensal microbes in contact with living human intestinal epithelial cells for more than a week in vitro and to analyze how gut microbiome, inflammatory cells, and peristalsis-associated mechanical deformations independently contribute to intestinal bacterial overgrowth and inflammation. This in vitro model replicated results from past animal and human studies, including demonstration that probiotic and antibiotic therapies can suppress villus injury induced by pathogenic bacteria. By ceasing peristalsis-like motions while maintaining luminal flow, lack of epithelial deformation was shown to trigger bacterial overgrowth similar to that observed in patients with ileus and inflammatory bowel disease. Analysis of intestinal inflammation on-chip revealed that immune cells and lipopolysaccharide endotoxin together stimulate epithelial cells to produce four proinflammatory cytokines (IL-8, IL-6, IL-1β, and TNF-α) that are necessary and sufficient to induce villus injury and compromise intestinal barrier function. Thus, this human gut-on-a-chip can be used to analyze contributions of microbiome to intestinal pathophysiology and dissect disease mechanisms in a controlled manner that is not possible using existing in vitro systems or animal models. 6 samples, 2 biological replicates for each 3 conditions.
2015-12-16 | E-GEOD-65790 | biostudies-arrayexpress
Project description:enzymes. However, many genes in the microbiome remain uncharacterized due to the challenge in culturing intestinal strains in vitro, which limits the identification of target enzymes. To address this issue, we developed an effective Activity-Based MetaProteomics (ABMP) strategy using a specific activity-based probe (ABP) to screen the entire gut microbiome for target enzymes, without the need to isolate and culture bacterial strains individually. α-Galactosidases (AGALs) are widely distributed in gut microbiota, plant, and animal kingdoms of life and have multiple applications in industries such as food, animal feed, and biomedical sectors. Despite the rich source of AGALs in the gut microbiome, many AGAL genes lack functional annotations. Using an activity-based cyclophellitol aziridine probe specific to AGAL, we successfully identified and characterized several new enzymes possessing AGAL activities from the gut microbiome.
| PXD044848 |
Project description:The gut microbiome is a malleable microbial community that can remodel in response to various factors, including diet, and contribute to the development of several chronic diseases, including atherosclerosis. We devised an in vitro screening protocol of the mouse gut microbiome to discover molecules that can selectively modify bacterial growth. This approach was used to identify cyclic D,L-α-peptides that remodeled the Western diet (WD) gut microbiome toward the low-fat-diet microbiome state. Daily oral administration of the peptides in WD-fed LDLr-/- mice reduced plasma total cholesterol levels and atherosclerotic plaques. Depletion of the microbiome with antibiotics abrogated these effects. Peptide treatment reprogrammed the microbiome transcriptome, suppressed the production of pro-inflammatory cytokines (including interleukin-6, tumor necrosis factor-α and interleukin-1β), rebalanced levels of short-chain fatty acids and bile acids, improved gut barrier integrity and increased intestinal T regulatory cells. Directed chemical manipulation provides an additional tool for deciphering the chemical biology of the gut microbiome and might advance microbiome-targeted therapeutics.
2019-12-31 | GSE104914 | GEO
Project description:The gut microbiome is a malleable microbial community that can remodel in response to various factors, including diet, and contribute to the development of several chronic diseases, including atherosclerosis. We devised an in vitro screening protocol of the mouse gut microbiome to discover molecules that can selectively modify bacterial growth. This approach was used to identify cyclic D,L-α-peptides that remodeled the Western diet (WD) gut microbiome toward the low-fat-diet microbiome state. Daily oral administration of the peptides in WD-fed LDLr-/- mice reduced plasma total cholesterol levels and atherosclerotic plaques. Depletion of the microbiome with antibiotics abrogated these effects. Peptide treatment reprogrammed the microbiome transcriptome, suppressed the production of pro-inflammatory cytokines (including interleukin-6, tumor necrosis factor-α and interleukin-1β), rebalanced levels of short-chain fatty acids and bile acids, improved gut barrier integrity and increased intestinal T regulatory cells. Directed chemical manipulation provides an additional tool for deciphering the chemical biology of the gut microbiome and might advance microbiome-targeted therapeutics.
2019-12-31 | GSE104913 | GEO
Project description:Background and Aims Interoceptive impacts on the brain triggered by changes in the intestinal microbial ecosystem influence mood-related behaviors such as anxiety and depression. Although changes in the gut microbiome can be driven by genetic mutations in the host, how alterations in the gut microbiome caused by host genetic variations affect behavioral outcomes is not fully understood. To investigate how host genetic variation affects interoceptive responses, we analyzed the gut microbiota and investigated gut–brain interactions in sirtuin 3 (Sirt3)-knockout (KO) mice. Methods We evaluated the composition of the gut microbiome and behavior in Sirt3-KO and wild-type (WT) mice. To distinguish microbiome-driven effects from genetic influences, we conducted cohousing experiments and compared results with heterozygous littermates. Region-specific changes in gene expression in the brain were identified by transcriptomic profiling of the limbic system. We also analyzed metabolites in the nucleus of the solitary tract (NTS) generated by gut microbiome–vagal signaling. The role of the vagus nerve in the gut-brain axis was further examined through vagotomy, alongside comparative choline analysis in both mood disorder patients and mice. Results Mood-related neurobehavioral changes and alterations in synaptic plasticity-related genes in the amygdala and bed nucleus of the stria terminalis (BNST) of Sirt3-KO mice appeared to be dependent on gut microbiome composition. Elevated plasma choline levels in both mood disorder patients and Sirt3-KO mice, together with reduced neurotransmitter-related metabolites (e.g., -aminobutyric acid [GABA] in the NTS), suggested that externalizing behaviors in Sirt3-KO mice are mediated by vagus nerve-dependent gut–brain axis signaling. Consistent with this, vagotomy abolished these changes, including GABA in the NTS, as well as alterations in synaptic plasticity in the amygdala and BNST. Conclusions Our findings suggest the novel finding that an altered gut microbiome caused by a host genetic change, namely a Sirt3 deficiency, is sensed in the NTS of the brain via the vagus nerve, leading to externalizing behaviors.
2025-10-09 | GSE305243 | GEO
Project description:A human gut-on-a-chip microdevice was used to coculture multiple commensal microbes in contact with living human intestinal epithelial cells for more than a week in vitro and to analyze how gut microbiome, inflammatory cells, and peristalsis-associated mechanical deformations independently contribute to intestinal bacterial overgrowth and inflammation. This in vitro model replicated results from past animal and human studies, including demonstration that probiotic and antibiotic therapies can suppress villus injury induced by pathogenic bacteria. By ceasing peristalsis-like motions while maintaining luminal flow, lack of epithelial deformation was shown to trigger bacterial overgrowth similar to that observed in patients with ileus and inflammatory bowel disease. Analysis of intestinal inflammation on-chip revealed that immune cells and lipopolysaccharide endotoxin together stimulate epithelial cells to produce four proinflammatory cytokines (IL-8, IL-6, IL-1β, and TNF-α) that are necessary and sufficient to induce villus injury and compromise intestinal barrier function. Thus, this human gut-on-a-chip can be used to analyze contributions of microbiome to intestinal pathophysiology and dissect disease mechanisms in a controlled manner that is not possible using existing in vitro systems or animal models.
2015-12-16 | GSE65790 | GEO
Project description:The intestinal microbiome forms dynamic ecosystem whose balanced composition and functioning are essential for maintaining overall gut health and well-being in living organisms. In broilers, dysbiosis disrupts the microbiota-host balance, often without obvious clinical symptoms but with intestinal inflammation, leading to impaired animal performance and significant economic losses. This study utilizes an in vivo model of dysbiosis to investigate the blood proteome response of broilers to intestinal imbalance. Microscopic histological changes in the gut (shorter villi, increased crypt depth, p<0.0001) were observed in the duodenal and jejunal tissue of challenged birds. Elevated levels of permeability markers faecal ovotransferrin (p < 0.0001) and serum iohexol (p= 0.0009) additionally indicated increased intestinal permeability in challenged group compared to control. The MS/MS-based proteomics analysis was performed on broilers’ blood plasma enabling identification of 388 proteins, 25 of which demonstrated significant difference between the groups. Functional analysis showed activation of immune response, signalling, and interspecies interaction, while proteins related to cellular physiology, cell-cell communication, and extracellular matrix (ECM) processes were suppressed. Protein-protein interaction (PPI) analysis revealed two clusters of downregulated proteins involved in ECM organization and cell adhesion. These results suggest that the dysbiosis challenge alters plasma protein expression as the host prioritizes immune defense over structural maintenance. The activation of immune processes and suppression of ECM pathways highlight potential biomarkers and therapeutic targets for addressing dysbiosis.
2025-07-14 | PXD056546 | Pride