Determining effects of microbial metabolite, Urolithin A on colon epithelial cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA453152 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7059080.fastq.gz | Fastqsanger.gz | |||
| SRR7059081.fastq.gz | Fastqsanger.gz | |||
| SRR7059082.fastq.gz | Fastqsanger.gz | |||
| SRR7059083.fastq.gz | Fastqsanger.gz | |||
| SRR7059084.fastq.gz | Fastqsanger.gz |
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Project description:Numerous studies signify that diets rich in phytochemicals reduce the risk of inflammatory bowel diseases (IBDs). However, their effects are often not uniform among individuals, possibly due to inter-individual variation in gut microbiota. The host indigenous gut microbiota and their metabolites have emerged as factors that greatly influence the efficacy of dietary interventions. The biological activities, mechanisms of actions and the specific targets of several microbial metabolites are unknown. Urolithin A (UroA) is one such natural microbial metabolite, which showed (including our recent study) anti-carcinogenic, anti-oxidative and anti-inflammatory activities. The goal of the experiment to determine if Urolithin A blocks the genes induced by lipopolysaccharide (mimicking bacterial effects on colon) as well as determine effects of Urolithin A alone.
2019-10-07 | GSE113581 | GEO
Project description:Briefly, this is a 28-day dietary intervention study participants will be asked to eat 2 ounces (52 grams) of walnuts every day for 3 weeks, and at the end of the study period they will come in for a colonoscopy. Participants will first start a 1-week run-in period where they will be asked to avoid foods high in ellagic acid. In addition, they will be asked to complete food surveys and two sets of 3-day dietary records, and to provide colon biopsies for this study during their routine colonoscopy, as well as a blood, and two urine and stool samples. Urine samples will be used for analysis of urolithin, ellagic acid metabolites. Stool samples will be used to assess gut microbiota changes after walnut consumption. Dietary records will be used for compliance and Food Frequency Questionnaire will be used to assess dietary habits. Lastly, the biopsy samples will be used for analysis of biomarkers and anti-inflammatory in the colon, as well as adherent microbiome to the colonic tissue. Data will be analyzed based on the urolithin phenotypes.
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Project description:Urolithin A, a natural gut microbial metabolite, exerts multiple beneficial effects upon supplementation, including prolonging lifespan, mitigating diseases, restoring the quality of aged oocytes and alleviating drug toxicity. The study aims to investigate the ovarian protective role of Urolithin A, focusing on its mechanisms for inhibiting primordial follicle activation and mitigating cyclophosphamide (CY)-induced follicle apoptosis. The results showed that Urolithin A significantly decreased the number of growing follicles, downregulated the expression of oocyte growth-related genes (Gdf9 and Zp3) and protein (DDX4), as well as Ki-67 and BrdU-positive signals. Further studies revealed that Urolithin A downregulated the levels of phosphorylated Akt and FOXO3a and decreased the percentage of oocytes with FOXO3a nuclear export. Molecular docking showed a strong binding ability between Urolithin A and its downregulated gene Pik3cg (PI3Kγ). Moreover, Urolithin A attenuated CY- and 4-HC-induced increases in Cleaved caspase-3 and cleaved PARP1 positive signals. Meanwhile, RNA-seq analysis indicated that Urolithin A downregulated CY-induced expression of DNA damage-related genes (Trp73 and Trim29). In short, Urolithin A inhibits primordial follicle activation by reducing PI3K/Akt pathway reactivity. Furthermore, Urolithin A prevents CY-induced follicle apoptosis. The study provides valuable insights into Urolithin A treatment for chemotherapy-induced infertility.
2025-07-30 | GSE299728 | GEO
Project description:Microbial metabolite ammonia disrupts CEACAM1-TGF-β signaling to promote colon cancer
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Project description:To investigate the effects of ppIAPP-GFP expression and urolithin B treatment in the gene expression of Saccharomyces cerevisiae cells, we compared different cells: cells expressing the empty vector, cells expressing ppIAPP-GFP, cells expressing the empty vector treated with urolithin B, cells expressing ppIAPP-GFP treated with urolithin B
2022-11-24 | GSE218152 | GEO
Project description:Urolithin A is a polyphenol derived from the multi-step metabolism of dietary ellagitannins by the human gut microbiota which can affect host health. Most, but not all, individuals harbor a microbiota capable of urolithin A production; however, the enzymes that dehydroxylate its dietary precursor, urolithin C, are unknown. Here, we used a combination of transcriptomics and proteomics to reveal a urolithin C dehydroxylase (ucd) operon that dehydroxylates 9-hydroxy urolithin compounds in Enterocloster spp. Using comparative genomics, we identified Lachnoclostridium pacaense as a novel urolithin C metabolizer. Biochemical characterization and structure predictions of proteins in the Ucd complex demonstrated that dehydroxylation was both NADH- and molybdopterin-dependent and used urolithin C as a terminal electron acceptor. A meta-analysis publicly available metagenomic data revealed that both bacteria and ucd operon genes are widely distributed in gut metagenomes and likely comprise keystone species in the metabolism of urolithins by the human gut microbiota.
2024-12-16 | PXD048514 | Pride
Project description:Clostridioides difficile is a Gram-positive, anaerobic, spore-forming bacterium responsible for antibiotic-associated pseudomembranous colitis. Clostridioides difficile infection (CDI) symptoms can range from diarrhea to life-threatening colon damage. Toxins produced by C. difficile (TcdA and TcdB) cause intestinal epithelial injury and lead to severe gut barrier dysfunction, stem cell damage, and impaired regeneration of the gut epithelium. Current treatment options for intestinal repair are limited. In this study, we demonstrate that treatment with the microbial metabolite urolithin A (UroA) attenuates CDI-induced adverse effects on the colon epithelium in a preclinical model of CDI-induced colitis. Moreover, our analysis suggests that UroA treatment protects against C. difficile-induced inflammation, disruption of gut barrier integrity, and intestinal tight junction proteins in the colon of CDI mice. Importantly, UroA treatment significantly reduced the expression and release of toxins from C. difficile without inducing bacterial cell death. These results indicate the direct regulatory effects of UroA on bacterial gene regulation. Overall, our findings reveal a novel aspect of UroA activity, as it appears to act at both the bacterial and host levels to protect against CDI-induced colitis pathogenesis. This research sheds light on a promising avenue for the development of novel treatments for C. difficile infection.IMPORTANCETherapy for Clostridioides difficile infections includes the use of antibiotics, immunosuppressors, and fecal microbiota transplantation. However, these treatments have several drawbacks, including the loss of colonization resistance, the promotion of autoimmune disorders, and the potential for unknown pathogens in donor samples. To date, the potential benefits of microbial metabolites in CDI-induced colitis have not been fully investigated. Here, we report for the first time that the microbial metabolite urolithin A has the potential to block toxin production from C. difficile and enhance gut barrier function to mitigate CDI-induced colitis.
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Project description:Urolithins are gut microbial metabolites derived from ellagitannins (ET) and ellagic acid (EA), and shown to exhibit anticancer, anti-inflammatory, anti-microbial, anti-glycative and anti-oxidant activities. Similarly, the parent molecules, ET and EA are reported for their neuroprotection and antidepressant activities. Due to the poor bioavailability of ET and EA, the in vivo functional activities cannot be attributed exclusively to these compounds. Elevated monoamine oxidase (MAO) activities are responsible for the inactivation of monoamine neurotransmitters in neurological disorders, such as depression and Parkinson's disease. In this study, we examined the inhibitory effects of urolithins (A, B and C) and EA on MAO activity using recombinant human MAO-A and MAO-B enzymes. Urolithin B was found to be a better MAO-A enzyme inhibitor among the tested urolithins and EA with an IC50 value of 0.88 µM, and displaying a mixed mode of inhibition. However, all tested compounds exhibited higher IC50 (>100 µM) for MAO-B enzyme.
| S-EPMC7345905 | biostudies-literature
Project description:Urolithins are gut microbial metabolites derived from ellagitannins (ET) and ellagic acid (EA), and shown to exhibit anticancer, anti-inflammatory, anti-microbial, anti-glycative and anti-oxidant activities. Similarly, the parent molecules, ET and EA are reported for their neuroprotection and antidepressant activities. Due to the poor bioavailability of ET and EA, the in vivo functional activities cannot be attributed exclusively to these compounds. Elevated monoamine oxidase (MAO) activities are responsible for the inactivation of monoamine neurotransmitters in neurological disorders, such as depression and Parkinson's disease. In this study, we examined the inhibitory effects of urolithins (A, B and C) and EA on MAO activity using recombinant human MAO-A and MAO-B enzymes. Urolithin B was found to be a better MAO-A enzyme inhibitor among the tested urolithins and EA with an IC50 value of 0.88 µM, and displaying a mixed mode of inhibition. However, all tested compounds exhibited higher IC50 (>100 µM) for MAO-B enzyme.
| S-EPMC7345905 | biostudies-literature