Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-47735
PROVIDER: PRJNA207540 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR891248_1.fastq.gz | Fastqsanger.gz | |||
| SRR891248_2.fastq.gz | Fastqsanger.gz | |||
| SRR891249_1.fastq.gz | Fastqsanger.gz | |||
| SRR891249_2.fastq.gz | Fastqsanger.gz | |||
| SRR891250_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 71 |
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Project description:Interplay of host microbiota, genetic perturbations, and inflammation promote local development of intestinal neoplasms in mice
2019-05-14 | E-GEOD-47735 | ExpressionAtlas
Project description:Interplay of host microbiota, genetic perturbations, and inflammation promotes local development of intestinal neoplasms in mice [BeadArray]
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Project description:Interplay of host microbiota, genetic perturbations, and inflammation promotes local development of intestinal neoplasms in mice [RNA-Seq]
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Project description:The preferential localization of some neoplasms, such as serrated polyps, in specific areas of the intestine suggests that non-genetic factors may be important for their development. To test this hypothesis, we took advantage of transgenic mice that expressed HB-EGF throughout the intestine, but develop serrated polyps only in the cecum. Here we show that a host-specific microbiome was associated with serrated polyps, and that alterations of the microbiota induced by antibiotic treatment or by embryo-transfer rederivation markedly inhibited the formation of serrated polyps in the cecum. Mechanistically, development of serrated polyps was associated with a local decrease in epithelial barrier-function, bacterial invasion, production of antimicrobials, and increased expression of several inflammatory factors such as IL-17, Cxcl2, Tnf-M-NM-1, and IL-1. Increased number of neutrophils were found within the serrated polyps, and their depletion significantly reduced polyp growth. Together these results indicate that non-genetic factors contribute to the development of serrated polyps and suggest that the development of these intestinal neoplasms in the cecum is driven by the interplay between genetic changes in the host, an inflammatory response, and a host-specific microbiota. Paired design; Surrounding and SP samples were obtained from the same mouse (n=3; mouse 1, 2, 3)
2014-02-12 | E-GEOD-47734 | biostudies-arrayexpress
Project description:The preferential localization of some neoplasms, such as serrated polyps, in specific areas of the intestine suggests that non-genetic factors may be important for their development. To test this hypothesis, we took advantage of transgenic mice that expressed HB-EGF throughout the intestine, but develop serrated polyps only in the cecum. Here we show that a host-specific microbiome was associated with serrated polyps, and that alterations of the microbiota induced by antibiotic treatment or by embryo-transfer rederivation markedly inhibited the formation of serrated polyps in the cecum. Mechanistically, development of serrated polyps was associated with a local decrease in epithelial barrier-function, bacterial invasion, production of antimicrobials, and increased expression of several inflammatory factors such as IL-17, Cxcl2, Tnf-α, and IL-1. Increased number of neutrophils were found within the serrated polyps, and their depletion significantly reduced polyp growth. Together these results indicate that non-genetic factors contribute to the development of serrated polyps and suggest that the development of these intestinal neoplasms in the cecum is driven by the interplay between genetic changes in the host, an inflammatory response, and a host-specific microbiota. SUMMARY: Serrated polyps (SP) are a heterogeneous group of neoplasms found in particular areas of the gut. To define the factors contributing to their specific localization, we analyzed a strain of transgenic mice that carry a genetic alteration throughout the intestinal epithelium, but only develop SP in the cecum. Transcriptome and immunostaining analyses showed increased expression of antimicrobial genes, inflammatory factors, and the presence of bacteria within SP. Alteration of the cecal microbiota by antibiotic treatment or by embryo-transfer rederivation dramatically reduced SP incidence. Microbiome analysis implicated a limited set of bacteria in the development of SP. Together, these results point to a crucial role for the microbiota in the localized development of SP in a genetically susceptible host. We obtained serrated polyp (SP) and surrounding normal (NM) tissue from the ceca of three affected mice (paired design) and assessed expression differences by RNA-Seq.
2014-02-12 | E-GEOD-47735 | biostudies-arrayexpress
Project description:The preferential localization of some neoplasms, such as serrated polyps, in specific areas of the intestine suggests that non-genetic factors may be important for their development. To test this hypothesis, we took advantage of transgenic mice that expressed HB-EGF throughout the intestine, but develop serrated polyps only in the cecum. Here we show that a host-specific microbiome was associated with serrated polyps, and that alterations of the microbiota induced by antibiotic treatment or by embryo-transfer rederivation markedly inhibited the formation of serrated polyps in the cecum. Mechanistically, development of serrated polyps was associated with a local decrease in epithelial barrier-function, bacterial invasion, production of antimicrobials, and increased expression of several inflammatory factors such as IL-17, Cxcl2, Tnf-α, and IL-1. Increased number of neutrophils were found within the serrated polyps, and their depletion significantly reduced polyp growth. Together these results indicate that non-genetic factors contribute to the development of serrated polyps and suggest that the development of these intestinal neoplasms in the cecum is driven by the interplay between genetic changes in the host, an inflammatory response, and a host-specific microbiota.
2014-02-12 | GSE47734 | GEO
Project description:The preferential localization of some neoplasms, such as serrated polyps, in specific areas of the intestine suggests that non-genetic factors may be important for their development. To test this hypothesis, we took advantage of transgenic mice that expressed HB-EGF throughout the intestine, but develop serrated polyps only in the cecum. Here we show that a host-specific microbiome was associated with serrated polyps, and that alterations of the microbiota induced by antibiotic treatment or by embryo-transfer rederivation markedly inhibited the formation of serrated polyps in the cecum. Mechanistically, development of serrated polyps was associated with a local decrease in epithelial barrier-function, bacterial invasion, production of antimicrobials, and increased expression of several inflammatory factors such as IL-17, Cxcl2, Tnf-α, and IL-1. Increased number of neutrophils were found within the serrated polyps, and their depletion significantly reduced polyp growth. Together these results indicate that non-genetic factors contribute to the development of serrated polyps and suggest that the development of these intestinal neoplasms in the cecum is driven by the interplay between genetic changes in the host, an inflammatory response, and a host-specific microbiota.
2014-02-12 | GSE47735 | GEO
Project description:The potential for commensal microorganisms indigenous to a host (the microbiome or microbiota) to alter infection outcome by influencing host-pathogen interplay is largely unknown. We used a multi-omics systems approach, incorporating proteomics, metabolomics, glycomics, and metagenomics, to explore the molecular interplay between the murine host, the pathogen Salmonella enterica serovar Typhimurium (S. Typhimurium), and commensal gut microorganisms during intestinal infection with S. Typhimurium. We find proteomic evidence that S. Typhimurium thrives within the infected 129/SvJ mouse gut without antibiotic pre-treatment, inducing inflammation and disrupting the intestinal microbiome (e.g., suppressing Bacteroidetes and Firmicutes while promoting growth of Salmonella and Enterococcus). Alteration of the host microbiome population structure was highly correlated with gut environmental changes, including the accumulation of metabolites normally consumed by commensal microbiota. Finally, the less characterized phase of S. Typhimurium's lifecycle was investigated, and both proteomic and glycomic evidence suggests S. Typhimurium may take advantage of increased fucose moieties to metabolize fucose while growing in the gut. The application of multiple omics measurements to Salmonella-induced intestinal inflammation provides insights into complex molecular strategies employed during pathogenesis between host, pathogen, and the microbiome.
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Project description:This is a mathematical model investigating the role of chronic inflammation in the development and progression of myeloproliferative neoplasms (MPNs). The model describes the proliferation from stem cells to mature cells, including mutations of healthy stem cells to become malignant stem cells. The model also features a simple inflammatory coupling coping with cell death and affecting the basic model beneath.
2024-09-02 | BIOMD0000000852 | BioModels
Project description:The mechanisms that mediate inflammatory macrophages in intestinal inflammation are incompletely understood. Here, using merged analysis of RNA sequences and mass spectrometry (MS)-based quantitative proteomics, we report the distinction of proteomics and transcriptomics in activated macrophage. Dipeptidase-2 (DPEP2), belonging to DPEP family, is highly expressed and downregulated sharply at protein level but not mRNA level in macrophages responding to inflammatory stimulations. Repression of DPEP2 not only enhances macrophage-mediated intestinal inflammation in vivo but also promotes the production of ROS and the transduction of inflammatory pathways in macrophages in vitro. Mechanistically, DPEP2 inhibits recruitment of inactivated macrophages to inflammatory sites by impairing activation of vimentin (VIM), and DPEP2 downregulation promotes the infiltration of pro-inflammatory macrophages through enhancing the activation of VIM by Akt1. Besides, overexpressed DPEP2 inhibits the transduction of inflammatory signals by resisting MAK3K7 in inactivated macrophages, and DPEP2 is degraded by activated Trim32 resulting in sharp activation of NF-κB and p38 MAPK signals by released MAK3K7 in pro-inflammatory macrophages during the development of intestinal inflammation. Trim32-DPEP2 axis accumulates potential energy of inflammation for macrophages. These results identify DPEP2 as a key regulator of macrophage-mediated intestinal inflammation. Thus, Trim32-DPEP2 axis may be a potential therapeutic target for intestinal inflammation.
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