Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1136812 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29856100_1.fastq.gz | Fastqsanger.gz | |||
| SRR29856100_2.fastq.gz | Fastqsanger.gz | |||
| SRR29856101_1.fastq.gz | Fastqsanger.gz | |||
| SRR29856101_2.fastq.gz | Fastqsanger.gz | |||
| SRR29856102_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 70 |
Similar Datasets
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: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: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: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: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:Inflammatory bowel disease (IBD) is characterized by dysbiosis of the gut microbiota and dysfunction of in testinal stem cells (ISCs). However, the direct interactions between IBD microbial factors and ISCs are unde scribed. Here, we identify α2A-adrenergic receptor (ADRA2A) as a highly expressed GPCR in ISCs. Through PRESTO-Tango screening, we demonstrate that tyramine, primarily produced by Enterococcus via tyrosine decarboxylase (tyrDC), serves as a microbial ligand for ADRA2A. Using an engineered tyrDC deficient Enterococcus faecalis strain and intestinal epithelial cell-specific Adra2a knockout mice, we show that Enterococcus-derived tyramine suppresses ISC proliferation, thereby impairing epithelial regeneration and exacerbating DSS-induced colitis through ADRA2A. Importantly, blocking the axis with an ADRA2A antagonist, yohimbine, disrupts tyramine-mediated suppression on ISCs and alleviates colitis.Our findings highlight a microbial ligand-GPCR pair in ISCs, revealing a causal link between microbial regulation of ISCs and colitis exacerbation and yielding a targeted therapeutic approach to restore ISC function in colitis.
2024-05-25 | GSE242865 | GEO
Project description:Inflammatory bowel diseases (IBD) are believed to be driven by dysregulated interactions between the host and the gut microbiota. Our goal is to characterize the relationships between mucosal T cells, the host tissue environment and microbial communities in IBD patients to identify new therapeutic targets. We identified 26 predictors from our combined data set that were effective in distinguishing between regions of the intestine undergoing active inflammation and regions that were normal. Network analysis on these 26 predictors revealed SAA1 as the most connected node linking the abundance of the genus Bacteroides with the production of IL17 and IL22 by CD4+ T cells. The SAA1-linked microbial and transcriptome interactions were further validated with data from the pediatric IBD RISK cohort. This study identifies expression of SAA1 as an important link between mucosal T cells, microbial communities and their tissue environment in IBD patients. A combination of FACS, gene expression and microbial profiling can distinguish between intestinal inflammatory states in IBD regardless of disease types.
2017-11-11 | GSE96665 | GEO
Project description:How pathogenesis of inflammatory bowel disease (IBD) depends on the complex interplay of host genetics, microbiome and the immune system is not fully understood. Here, we showed that Downstream of Kinase 3 (DOK3), an adaptor protein involved in immune signaling, confers protection of mice from dextran sodium sulfate (DSS)-induced colitis. DOK3-deficiency promotes gut microbial dysbiosis and enhanced colitis susceptibility, which can be reversed by the transfer of normal microbiota from wild-type mice. Mechanistically, DOK3 exerts its protective effect by suppressing JAK2/STAT3 signaling in colonic neutrophils to limit their S100a8/9 production, thereby maintaining gut microbial ecology and colon homeostasis. Hence, our findings reveal that the immune system and microbiome function in a feed-forward manner, whereby DOK3 maintains colonic neutrophils in a quiescent state to establish a gut microbiome essential for intestinal homeostasis and protection from IBD.
2021-11-10 | GSE186597 | GEO
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
Project description:Defects in RNA splicing have been linked to numerous human disorders, but remain poorly explored in inflammatory bowel disease (IBD). Here, we report that, in the gut epithelium of patients with ulcerative colitis (UC), the expression of the chromatin and alternative splicing regulator HP1g is strongly reduced. Accordingly, inactivation of the HP1g gene in the mouse gut triggered several IBD-like traits, including inflammation and dysbiosis. In parallel, we discovered that its loss of function broadly increased splicing noise, reducing requirement for canonical splicing consensus sequences, and favoring the usage of cryptic splice sites at numerous genes with key functions in gut biology. This notably resulted in the production of progerin, a noncanonical toxic splice variant of prelamin A mRNA, responsible for the Hutchinson Gilford Progeria Syndrome (HGPS) of premature aging. Likewise, production of progerin transcript was found to be a signature of colonic cells from UC patients. Thus, our study identifies HP1g as a regulator of RNA metabolism in vivo, providing a unique mechanism linking anti-inflammation and accuracy of RNA splicing in the gut epithelium. HP1 defect may confer a general disturbance in RNA splicing precision to scrutinize in IBD and more generally in accelerating aging diseases.
2022-10-25 | PXD031580 | Pride