Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expansion of bacteriophages during disease worsens intestinal inflammation and colitis

ABSTRACT: Expansion of bacteriophages during disease worsens intestinal inflammation and colitis

PROVIDER: PRJNA510809 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8354400.fastq.gz	Fastqsanger.gz
	SRR8354401.fastq.gz	Fastqsanger.gz
	SRR8354402.fastq.gz	Fastqsanger.gz
	SRR8354403.fastq.gz	Fastqsanger.gz
	SRR8354404.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 9

Similar Datasets

Expansion of bacteriophages during disease worsens intestinal inflammation and colitis

Project description:Expansion of bacteriophages during disease worsens intestinal inflammation and colitis

| PRJNA510809 | ENA

Expansion of bacteriophages during disease worsens intestinal inflammation and colitis

Project description:Purified phage was used to prevent tumor growth in a mouse model of bacteria aggravated-colorectal cancer. Composite E. coli phage or vehicle control was added to the drinking water of specific pathogen free (SPF) APCmin mice and animals were colonized with E.coli NC101. APCmin mice displayed no overall difference in the number of tumors that formed within the small intestine, however colonization with E. coli NC101 accelerated the growth of tumors resulting in a significant increase in large tumor formation. Importantly, bacteriophage treatment of AIEC colonized APCmin animals significantly reduced E. coli colonization.

2019-03-01 | GSE124123 | GEO

Expansion of Bacteriophages Is Linked to Aggravated Intestinal Inflammation and Colitis.

Project description:Bacteriophages are the most abundant members of the microbiota and have the potential to shape gut bacterial communities. Changes to bacteriophage composition are associated with disease, but how phages impact mammalian health remains unclear. We noted an induction of host immunity when experimentally treating bacterially driven cancer, leading us to test whether bacteriophages alter immune responses. Treating germ-free mice with bacteriophages leads to immune cell expansion in the gut. Lactobacillus, Escherichia, and Bacteroides bacteriophages and phage DNA stimulated IFN-γ via the nucleotide-sensing receptor TLR9. The resultant immune responses were both phage and bacteria specific. Additionally, increasing bacteriophage levels exacerbated colitis via TLR9 and IFN-γ. Similarly, ulcerative colitis (UC) patients responsive to fecal microbiota transplantation (FMT) have reduced phages compared to non-responders, and mucosal IFN-γ positively correlates with bacteriophage levels. Bacteriophages from active UC patients induced more IFN-γ compared to healthy individuals. Collectively, these results indicate that bacteriophages can alter mucosal immunity to impact mammalian health.

| S-EPMC6885004 | biostudies-literature

Bacteriophages

Project description:Bacteriophages targeting human gut bacteria

| PRJNA860708 | ENA

Deubiquitinase OTUD6A in macrophages promotes intestinal inflammation and colitis via deubiquitination of NLRP3

Project description:Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract, which has been shown to increase the incidence of colorectal cancer. Recent studies have highlighted the role of ubiquitination, a post-translational modification, in the occurrence and development of colonic inflammation. Ovarian tumor deubiquitinase 6A (OTUD6A) is a deubiquitinating enzyme, which regulates cell proliferation and tumorigenesis. In this study, we investigated the expression and role of OTUD6A in IBD. Wide-type or Otud6a-/- mice were used to develop dextran sodium sulfate (DSS)- or 2,6,4-trinitrobenzene sulfonic acid (TNBS)-induced colitis model, as well as azoxymethane (AOM)/DSS-induced colitis-associated cancer model. Bone marrow-derived macrophages (BMDMs) were isolated from wild-type and Otud6a-/- mice to dissect molecular mechanisms. Our data show that OTUD6A deficiency attenuated DSS or TNBS-induced colitis, as well as AOM/DSS-induced colitis-related colon cancer in vivo. Bone marrow transplantation experiments further revealed that OTUD6A in myeloid cells was responsible for exacerbation of DSS-induced colitis. Mechanistically, OTUD6A directly bound to NACHT domain of NLRP3 inflammasome and selectively cleaved K48-linked polyubiquitin chains from NLRP3 at K430 and K689 to enhance the stability of NLRP3, leading to increased IL-1β level and inflammation. Taken together, our research identifies a new function of OTUD6A in the pathogenesis of colitis by promoting NLRP3 inflammasome activation, suggesting that OTUD6A could be a potential target for the treatment of IBD.

2023-04-01 | GSE224239 | GEO

Comparative genomic hybridization of DNA from bacteriophages from Bartonella grahamii and cellular DNA

Project description:The DNA content of bacteriophages from Bartonella grahamii was investigated by hybridization against cellular DNA from the same organism. Phage particles were isolated from plate grown bacteria as well as from different growth phases during culture in liquid medium.

2009-07-04 | E-MEXP-2149 | biostudies-arrayexpress

Examining the brain's response to intestinal permeability and inflammation in the dextran sulfate sodium-induced colitis model.

Project description:The gut and brain are increasingly linked in human disease, with neuropsychiatric conditions classically long attributed to the brain showing an involvement of the intestine and inflammatory bowel diseases displaying an ever-lengthening list of neurological comorbidities. To identify molecular systems that underpin this gut-brain connection and thus discover therapeutic targets, experimental models of gut dysfunction must be evaluated for brain effects. In the present study, we examine disturbances along the gut-brain axis in a widely used murine model of colitis, the dextran sodium sulfate (DSS) model, using high-throughput transcriptomics and an unbiased network analysis strategy coupled with standard outcome measures, yielding a comprehensive approach to identify key disease processes in both colon and brain. We examine the reproducibility of colitis induction with this model and its resulting genetic programs during different phases of disease, finding that DSS-induced colitis is largely reproducible with a few site-specific molecular features. We focus on the circulating immune system, which exhibits an activation of pro-inflammatory innate immunity during colitis, as the vessel between gut and brain. Our unbiased approach provides supporting evidence for immune activation in the brain during colitis, suggests that myelination may be a vulnerable system with intestinal permeability, and identifies a possible role for oxidative stress and brain oxygenation. Overall, we provide a comprehensive evaluation of multiple systems in a prevalent experimental model of intestinal permeability, which will inform future studies using this model and others, assist in the identification of druggable targets, and contribute to our understanding of the concomitance of intestinal and neuropsychiatric dysfunction.

2023-08-01 | GSE239820 | GEO

Anatabine ameliorates intestinal inflammation and reduces the production of pro-inflammatory factors in a dextran sulfate sodium mouse model of colitis.

Project description:Objective: In this study, we aimed to evaluate the anti-inflammatory properties of nicotine and anatabine in a dextran sulfate sodium (DSS) mouse model of ulcerative colitis (UC). Methods: C57BL/6 male mice (10 groups with 8 animals each) were orally administered nicotine at a concentration of 5 or 20 mg/kg body weight or anatabine at a concentration of 5 or 20 mg/kg body weight for a total of 21 days. Colitis was induced by oral administration of 3.5% DSS in drinking water ad libitum during days 14–21. Colonic samples were collected for transcriptomic analysis and multi-analyte profiling (MAP). Results: Oral administration of anatabine, but not nicotine, reduced the clinical symptoms of DSS-induced colitis. The result of gene expression analysis suggested that anatabine had a restorative effect on global DSS-induced gene expression profiles, while nicotine only had limited effects. Accordingly, MAP findings revealed that anatabine reduced the colonic abundance of DSS-associated cytokines and increased IL‑10 abundance. Conclusions: Our results support the reduction of inflammatory effects by anatabine in the DSS mouse model of UC.

2020-11-03 | E-MTAB-8543 | biostudies-arrayexpress

Caulobacter bacteriophages

Project description:Multiple Caulobacter bacteriophages from environmental sources. Genome sequencing and assembly

| PRJNA396547 | ENA

Bacteriophages genome sequencing

Project description:sequencing bacteriophages genome isolated from environment samples

| PRJEB52972 | ENA