PMID: 26843508 RUN1
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PROVIDER: PRJEB30375 | ENA |
REPOSITORIES: ENA
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Project description:Fungal microbiota dysbiosis in IBD PMID: 26843508 RUN2
| PRJEB30379 | ENA
Project description:Fungal microbiota dysbiosis in IBD PMID: 26843508 RUN3
| PRJEB30381 | 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:Microbial dysbiosis has been identified in adult inflammatory bowel disease (IBD) patients. However, microbial composition and functional interplay between host genetics and microorganisms in early IBD onset remain poorly defined. Here, we identified and demonstrated the causal effect of Atopobium parvulum and the gut microbiota in pediatric IBD. Microbiota and proteomic profiling revealed that the abundance of A. parvulum, a potent H2S producer, was associated with increased disease severity and a concurrent reduction in the expression of the host H2S detoxification pathway. In the Il10-/- mouse model of inflammation, A. parvulum induced severe pancolitis that was dependent on the presence of the gut microbiota. In addition, we demonstrated that administration of bismuth, an H2S scavenger, prevented A. parvulum-induced colitis. Our findings identified Atopobium parvulum as a major mediator of inflammation severity, and revealed an alteration of the balance between the production and detoxification of H2S in the gastrointestinal tract.
2022-02-22 | PXD000690 | Pride
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.
2016-06-01 | E-MTAB-3723 | biostudies-arrayexpress
Project description:Liver injury is a common complication of inflammatory bowel disease (IBD). However, the mechanisms of liver injury development are not clear in IBD patients. Gut microbiota is thought to be engaged in IBD pathogenesis. Here, by an integrated analysis of host transcriptome and colonic microbiome, we have attempted to reveal the mechanism of liver injury in colitis mice. In this study, dextran sulfate sodium (DSS) -induced mice colitis model was constructed. Liver and colon transcriptome results showed that immune response and lipid metabolism-related pathways were dramatically altered, while DNA damage repair-related pathways were only significantly down-regulated in the colon. The microbiota of DSS-treated mice underwent strong transitions. Correlation analyses identified genes associated with liver and colon injury, whose expression was associated with the abundance of liver and gut health-related bacteria Collectively, the results indicate that the liver injury in colitis mice may be related to the intestinal dysbiosis and host-microbiota interactions. These findings may provide new insights for identifying potential targets for the treatment of IBD and its induced liver injury.
2021-08-16 | GSE181959 | GEO
Project description:The human intestinal microbiota plays an essential role in host health. Modifications in its composition and diversity could induce pathologies such as inflammatory bowel diseases (IBD). These diseases are characterized by an unbalanced intestinal microbiota (a process known as dysbiosis) and an altered immune response. Faecalibacterium prausnitzii, the most abundant commensal bacterium in the human intestinal microbiota of healthy individuals (representing more than 5% of the total bacterial population), has been reported to be lower in feces and mucosa-associated microbiota of IBD patients. In addition, we have shown that both F. prausnitzii and its culture supernatant (SN) have anti-inflammatory and protective effects in both acute and chronic colitis models. However, the host molecular mechanisms involved in these anti-inflammatory effects remain unknown. In order to address this issue, we performed DNA chip-based transcriptomic analyses in HT-29 human intestinal epithelial cells stimulated with TNF-a and exposed to F. prausnitzii SN or to BHI (growth medium for F prausnitzii).
2020-11-02 | GSE72048 | GEO
Project description:In the DSS-induced colitis model, the epithelial damage and resulting inflammation is restricted to the colon, with a potential influence on the microbial composition in the adjacent cecum. Several studies have reported changes of the gut microbiota in the DSS-induced colitis model and other mouse models of IBD. Furthermore, metaproteomics analysis of the gut microbiome in a mouse model of Crohn’s disease demonstrated that disease severity and location are microbiota-dependent, with clear evidence for the causal role of bacterial dysbiosis in the development of chronic ileal inflammation. We have developed a refined model of chronic DSS-induced colitis that reflects typical symptoms of human IBD without a risky body weight loss usually observed in DSS models [Hoffmann et al., submitted]. In this study, we used metaproteomics to characterize the disease-related changes in bacterial protein abundance and function in the refined model of DSS-induced colitis. To assess the structural and functional changes, we applied 16S rRNA gene sequencing and metaproteomics analysis of the intestinal microbiota in three different entities of the intestinal environment, i.e. colon mucus, colon content and cecum content.
2020-03-17 | PXD007220 | Pride
Project description:Most preclinical models of IBD were developed in mice which share 85% genomic homology with humans and are genetically tractable. However, rats have historically been the model of choice for immunologic, cardiovascular, and neurologic diseases because they more closely recapitulate human physiology6. Recent work on the role of microbial dysbiosis in IBD has also shown that rat microbiota is more closely related to those of humans than mice7. Taken together, this suggests that a single preclinical model may not be optimal for delineating the molecular pathways involved in IBD pathogenesis. Previous research in rat models of IBD have focused primarily on characterization of clinical score and histopathological findings8, with a lack of systematic investigation into potential molecular pathways affected, thereby making it difficult to integrate this model with other preclinical and clinical research. In the current study, we have undertaken a systematic transcriptomic analysis of a rat model of experimental colitis along with a three-way comparison between an established mouse preclinical model and available human clinical datasets in an effort to identify conserved immunological pathways in IBD.
2023-11-06 | GSE245994 | GEO