Fungal microbiota dysbiosis in IBD PMID: 26843508 RUN3
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PROVIDER: PRJEB30381 | ENA |
REPOSITORIES: ENA
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Project description:Fungal microbiota dysbiosis in IBD PMID: 26843508 RUN1
| PRJEB30375 | ENA
Project description:Fungal microbiota dysbiosis in IBD PMID: 26843508 RUN2
| PRJEB30379 | ENA
Project description:Fungal microbiota dysbiosis in IBD_16s data
| PRJEB30383 | ENA
Project description:Dysbiosis is linked to the pathogenesis of inflammatory bowel disease. Although there is a lot of interest in restoring the balance, we do not understand the effects of dysbiosis, especially on epithelial cells. In addition, we know that epithelial cells from IBD patients maintain intrinsic defects. For that reason, we aimed to unravel if epithelial cells of UC patients are more sensitive towards microbiota stimulation, compared to non-IBD controls. In addition, we analyzed the effect of UC microbiota or microbiota of healthy donors towards epithelial cells. Confluent organoid derived monolayers of 8 UC patients and 8 non-IBD controls were co-cultured for 6 hours with microbiota (3.10^8 cells) , derived of a healthy donor (HD) or UC patients. If applicable, epithelial cells were first cultured for 24 hours with an inflammatory mix (100 ng/mL TNFα, 20 ng/mL IL1β, 1 µg/mL Flagellin). The inflammatory stimulation was continued in the 6 hours co-culture.Transcriptomic expression of epithelial cells was evaluated after 6 hours co-culture by Truseq for Illumina.
2022-07-31 | E-MTAB-10832 | biostudies-arrayexpress
Project description:Gut dysbiosis is closely involved in the pathogenesis of inflammatory bowel disease (IBD). However, it remains unclear whether IBD-associated gut dysbiosis plays a primary role in disease manifestation or is merely secondary to intestinal inflammation. Here, we established a humanized gnotobiotic (hGB) mouse system to assess the functional role of gut dysbiosis associated with two types of IBD - Crohn's disease (CD) and ulcerative colitis (UC). In order to explore the functional impact of dysbiotic microbiota in IBD patients on host immune responses, we analyzed gene expression profiles in colonic mucosa of hGB mice colonized with healty (HC), CD, and UC microbiota.
2015-10-10 | GSE73882 | GEO
Project description: Not available
| S-EPMC5532459 | biostudies-literature
Project description:The goal of this project is to find out whether human intestinal IgA1 and IgA2 secretion, transport and reactivity towards the microbiota might be involved in dysbiosis induction during Crohn’s disease and Ulcerative colitis. Mass spectrometry was used to characterize SIgA from Crohn’s disease patient and Ulcerative colitis patient, in term of O- and N-glycosylation in order to study their reverse transcytosis capacity and their role in intestinal inflammation.
2022-06-27 | PXD024060 | Pride
Project description:The period from birth to two years is the phase of the fastest growth and development in children, as well as an important window for the development of intestinal microbiota. Dysbiosis of the gut microbiome can lead to various adverse conditions in children, including malabsorption and immune abnormalities, ultimately resulting in a series of negative events related to growth and development. Lysine acetylation, as a significant post-translational modification, plays a complex and crucial role in the regulation of gut microbiota. This study aims to investigate the mechanism by which ABX-induced lysine acetylation affects the abnormal physiological state simulating gut microbiota dysbiosis in children. In this study, we identified a total of 16,579 acetylation sites from 5,218 proteins. We found that antibiotic-induced dysbiosis in young mice (3 weeks) can cause extensive changes in the lysine acetylation and proteomic profiles of cecal tissue. Differentially acetylated proteins are involved in various metabolic pathways, including the citrate cycle (TCA) cycle, butanoate metabolism, pyruvate metabolism, glycolysis/gluconeogenesis, and fatty acid biosynthesis. These differential acetylation sites are distributed across the cytoplasm, nucleus, and mitochondria, suggesting that multiple cellular functions are involved in regulation. Our findings suggest that early-life gut microbiota dysbiosis may lead to a series of metabolic disorders by regulating lysine acetylation in cecal tissue, resulting in delayed growth and development. This study aims to provide valuable insights into the molecular mechanisms underlying a series of pathophysiological processes caused by early-life gut microbiota dysbiosis. It contributes to a deeper understanding of the consequences of acetylation changes associated with early-life gut microbiota dysbiosis and its potential role in metabolic disorders.
2025-09-15 | PXD064558 | Pride
Project description:Background: Schizophrenia (SZ) is a chronic, severe mental disorder that presents significant challenges to diagnosis and effective treatment. Emerging evidence suggests that gut microbiota may play a role in the disease's pathogenesis. However, fewer studies have directly investigated the potential links between oral microbiota and SZ. Purpose: This study aimed to explore the relationship between salivary microbiota dysbiosis and SZ, examining microbial and metabolic alterations that may contribute to SZ pathophysiology. Methods: Salivary samples from 30 hospitalized patients diagosed with SZ and 10 healthy controls were collected. The microbial and metabolic profiles were analyzed using 16S rRNA gene sequencing and metabolomic profiling. Clinical parameters, including oral health status, were also evaluated to minimize variability in sampling. Results: Patients with SZ exhibited significantly poorer oral health compared to healthy controls, with more missing teeth and worse periodontal status. Microbiota sequencing revealed notable alterations in the overall structure and composition of the salivary microbiome in SZ patients, characterized by increased abundance of specific genera such as Neisseria and Porphyromonas. Metabolomic analysis indicated significant differences between the SZ and control groups, with upregulation of key metabolic pathways, including “β-alanine metabolism” and “vitamin digestion and absorption”. Correlations between microbial dysbiosis and elevated levels of certain metabolites, such as L-methionine sulfoxide (L-MetO) and tyramine, were observed, suggesting links to oxidative stress. Conclusion: The study highlights the presence of significant dysbiosis and metabolic dysfunction in the salivary microbiota of SZ patients, suggesting that alterations in the oral microbiome may contribute to SZ pathogenesis. These results provide new insights into potential diagnostic biomarkers and therapeutic targets for SZ. Further studies with larger sample sizes are required to validate these findings.
2025-11-27 | GSE283329 | GEO
Project description:DNA methylation profile of mouse sperm from conventionally-raised mice and gut dysbiosis experienced mice were characterized using whole-genome bisulfite sequencing. Genome-wide DNA methylation changes between control and dysbiotic male�s sperm were highly comparable, with no change in DNAme globally or at genomic features, only 21 differentially methylated regions (DMR) were identified, which did not overlap known regulatory elements. Epididymal sperm samples were harvested from 11 weeks old inbred male mice that were experiencing gut microbiota dysbiosis for 6-week (antibiotics treated, n=5), or drink sterilized water (control, n=5).
2023-11-13 | E-MTAB-10033 | biostudies-arrayexpress