CS-Permeability
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB81708 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Background: Alcohol misuse, binge drinking pattern, and gender-specific effects in the middle-aged population has been clearly underestimated. In the present study, we focused on understanding gender-specific effects of alcohol exposure on the gut-liver axis and the role of gut microbiota in modulating gender-specific responses to alcohol consumption. Methods: Fifty-two-week-old female and male C57BL/6 mice were fasted for 12 h, and then administered a single oral dose of ethanol (EtOH) (6 g/kg). Controls were given a single dose of PBS. Animals were sacrificed 8 h later. Alternatively, fecal microbiota transplantation (FMT) was performed in 52-week-old male mice from female donors of the same age. Permeability of the large intestine (colon), gut microbiota, liver injury, and inflammation was thoroughly evaluated in all groups. Results: Middle-aged male mice exposed to EtOH showed a significant increase in gut permeability in the large intestine, evaluated by FITC-dextran assay and ZO-1, OCCLUDIN and MUCIN-2 immuno-staining, compared to PBS-treated animals, whilst female mice of the same age also increased their gut permeability, but displayed a partially maintained intestinal barrier integrity. Moreover, there was a significant up-regulation of TLRs and markers of hepatocellular injury, cell death (AST, TUNEL-positive cells) and lipid accumulation (ORO) in male mice after EtOH exposure. Interestingly, FMT from female donors to male mice reduced gut leakiness, modified gut microbiota composition, ameliorated liver injury and inflammation, TLR activation and the senescence phenotype of middle-aged mice. Conclusion: Our findings highlighted the relevance of gender in middle-aged individuals who are exposed to alcohol in the gut-liver axis. Moreover, our study revealed that gender-specific microbiota transplantation might be a plausible therapy in the management of alcohol-related disorders during aging.
2024-04-18 | GSE263477 | GEO
Project description:Gut microbiota are known to influence oral drug disposition, yet the specific host pathways they affect remain poorly characterized. This study provides a transcriptome-wide characterization of how physiological gut microbiota regulate the expression of intestinal transporters, phase I and phase II metabolic enzymes, and barrier machinery relevant to oral drug disposition. By identifying microbiota-responsive processes, this work defines the scope of inter-individual variability attributable to gut microbial effects.
2026-01-31 | GSE317716 | GEO
Project description:Intracerebral hemorrhage (ICH) induces alterations in the gut microbiota composition, significantly impacting neuroinflammation post-ICH. However, the impact of gut microbiota absence on neuroinflammation following ICH-induced brain injury remain unexplored. Here, we observed that the gut microbiota absence was associated with reduced neuroinflammation, alleviated neurological dysfunction, and mitigated gut barrier dysfunction post-ICH. In contrast, recolonization of microbiota from ICH-induced SPF mice by transplantation of fecal microbiota (FMT) exacerbated brain injury and gut impairment post-ICH. Additionally, microglia with transcriptional changes mediated the protective effects of gut microbiota absence on brain injury, with Apoe emerging as a hub gene. Subsequently, Apoe deficiency in peri-hematomal microglia was associated with improved brain injury. Finally, we revealed that gut microbiota influence brain injury and gut impairment via gut-derived short-chain fatty acids (SCFA).
2024-05-13 | GSE266602 | GEO
Project description:Accumulating evidence indicates that gut microbiota dysbiosis is associated with increased blood-brain barrier (BBB) permeability and contributes to Alzheimer’s disease (AD) pathogenesis. In contrast, the influence of gut microbiota on the blood-cerebrospinal fluid (CSF) barrier has not yet been studied. Here, RNA-seq analysis of choroid plexus tissues of normal colonized specific pathogen-free (SPF) versus decolonized antibiotics-treated mice revealed that the barrier function of choroid plexus is affected by the absence of gut microbiota in the AB mice.
2023-06-05 | GSE228655 | GEO
Project description:Morphine and its pharmacological derivatives are the most prescribed analgesics for moderate to severe pain management. However, chronic use of morphine reduces pathogen clearance and induces bacterial translocation across the gut barrier. The enteric microbiome has been shown to play a critical role in the preservation of the mucosal barrier function and metabolic homeostasis. Here, we show for the first time, using bacterial 16s rDNA sequencing, that chronic morphine treatment significantly alters the gut microbial composition and induces preferential expansion of the gram-positive pathogenic and reduction of bile-deconjugating bacterial strains. A significant reduction in both primary and secondary bile acid levels was seen in the gut, but not in the liver with morphine treatment. Morphine induced microbial dysbiosis and gut barrier disruption was rescued by transplanting placebo-treated microbiota into morphine-treated animals, indicating that microbiome modulation could be exploited as a therapeutic strategy for patients using morphine for pain management. In this study, we establish a link between the two phenomena, namely gut barrier compromise and dysregulated bile acid metabolism. We show for the first time that morphine fosters significant gut microbial dysbiosis and disrupts cholesterol/bile acid metabolism. Changes in the gut microbial composition is strongly correlated to disruption in host inflammatory homeostasis13,14 and in many diseases (e.g. cancer/HIV infection), persistent inflammation is known to aid and promote the progression of the primary morbidity. We show here that chronic morphine, gut microbial dysbiosis, disruption of cholesterol/bile acid metabolism and gut inflammation; have a linear correlation. This opens up the prospect of devising minimally invasive adjunct treatment strategies involving microbiome and bile acid modulation and thus bringing down morphine-mediated inflammation in the host.
2016-06-01 | E-MTAB-3722 | biostudies-arrayexpress
Project description:Healthy aging relies on a symbiotic host–microbiota relationship. The age-associated decline of the immune system can pose a threat in this delicate equilibrium. In this work, we investigated how the functional deterioration of T cells can impact host–microbiota symbiosis and gut barrier integrity and the implications of this deterioration for inflammaging, senescence, and health decline. Using the Tfamfl/flCd4Cre mouse model, we found that T cell failure compromised gut immunity leading to a decrease in T follicular and regulatory T (Treg) cells and an accumulation of highly proinflammatory and cytotoxic T cells. These alterations were associated with intestinal barrier disruption and gut dysbiosis. Microbiota depletion or adoptive transfer of total CD4 T cells or a Treg cell–enriched pool prevented gut barrier dysfunction and mitigated premature inflammaging and senescence, ultimately enhancing healthspan in this mouse model. Thus, a competent CD4 T cell compartment is critical to ensure healthier aging by promoting host–microbiota mutualism and gut barrier integrity.
2025-08-04 | GSE266095 | GEO
Project description:Healthy aging relies on a symbiotic host–microbiota relationship. The age-associated decline of the immune system can pose a threat in this delicate equilibrium. In this work, we investigated how the functional deterioration of T cells can impact host–microbiota symbiosis and gut barrier integrity and the implications of this deterioration for inflammaging, senescence, and health decline. Using the Tfamfl/flCd4Cre mouse model, we found that T cell failure compromised gut immunity leading to a decrease in T follicular and regulatory T (Treg) cells and an accumulation of highly proinflammatory and cytotoxic T cells. These alterations were associated with intestinal barrier disruption and gut dysbiosis. Microbiota depletion or adoptive transfer of total CD4 T cells or a Treg cell–enriched pool prevented gut barrier dysfunction and mitigated premature inflammaging and senescence, ultimately enhancing healthspan in this mouse model. Thus, a competent CD4 T cell compartment is critical to ensure healthier aging by promoting host–microbiota mutualism and gut barrier integrity.
2025-08-04 | GSE281677 | GEO
Project description:The ERC “MINERVA” project (GA 724734) aims at developing a multi-organ-on-a-chip engineered platform to recapitulate in vitro the main players involved in the MGBA crosstalk: the microbiota, the gut epithelium, the immune system, the blood-brain barrier and the brain. In this context, the gut epithelium represents a physiological barrier that separates the intestinal lumen from the systemic circulation, and in several pathological circumstances, seems that its permeability might significantly increase and allow the passage of biologically active molecules into the blood vessels surrounding the intestinal mucosa. In the present work, we present our MINERVA 2.0 device and our innovative gut-on-a-chip device obtained by culturing in MINERVA 2.0 and a human gut epithelial CaCo2 cell based model. In particular, we have cultured the cells under perfusion and have assessed cell behavior by addressing cellular viability, tight junction imaging, apparent permeability by FITC-Dextran and transepithelial electrical resistance evaluation. Transcriptomic profile was used to further elucidate the effects of dynamic perfusion on Caco-2 cells.
2022-10-31 | E-MTAB-11949 | biostudies-arrayexpress
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:We have previously demonstrated that the gut microbiota can play a role in the pathogenesis of conditions associated with exposure to environmental pollutants. It is well accepted that diets high in fermentable fibers such as inulin can beneficially modulate the gut microbiota and lessen the severity of pro-inflammatory diseases. Therefore, we aimed to test the hypothesis that hyperlipidemic mice fed a diet enriched with inulin would be protected from the pro-inflammatory toxic effects of PCB 126.
2020-02-27 | E-MTAB-8798 | biostudies-arrayexpress