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RNA sequencing of the stomachs of H. pylori-infected WT and Mincle–/– mice after 8 weeks

ABSTRACT: RNA sequencing of the stomachs of H. pylori-infected WT and Mincle–/– mice after 8 weeks

PROVIDER: PRJNA561590 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10013135.fastq.gz	Fastqsanger.gz
	SRR10013136.fastq.gz	Fastqsanger.gz
	SRR10013137.fastq.gz	Fastqsanger.gz
	SRR10013138.fastq.gz	Fastqsanger.gz
	SRR10013139.fastq.gz	Fastqsanger.gz

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Similar Datasets

RNA sequencing of the stomachs of H. pylori-infected WT and Mincle–/– mice after 8 weeks

Project description:Helicobacter pylori (H. pylori) causes assorted gastrointestinal disorders. H. pylori-specific T cells develop during infection, which is a prerequisite for the induction of gastritis and malignancy. How the innate immune system senses H. pylori to prime T cells remains unclear. We report that cholesteryl glucosides in H. pylori activate innate immunity through C-type lectin receptors (CLRs). Cholesteryl acyl α-glucoside (αCAG) was identified as a ligand for Mincle (Clec4e). Upon H. pylori infection, T cell responses and gastritis were ameliorated in Mincle-deficient mice, although bacterial numbers were comparable.Thus the cholesteryl lipid–CLR axis exacerbates H. pylori-induced gastric inflammation with limited contribution to protective immunity.

2020-09-19 | GSE136203 | GEO

RNA sequencing of the stomachs of H. pylori-infected mice after 8 weeks

Project description:RNA sequencing of the stomachs of H. pylori-infected mice after 8 weeks

| PRJNA963900 | ENA

RNA sequencing of the stomachs of H. pylori-infected mice after 8 weeks

Project description:The aim of this study is to identify alterations induced in gastric mucosa of mice infected with Helicobacter pylori, in order to identify genes that associated to the infection on gastric lesions.

2023-05-04 | GSE231337 | GEO

Expression data from 6-month Helicobacter felis-infected WT and Gli1-/- mouse stomachs

2013-01-24 | GSE43693 | GEO

Gastric single-cell RNA-sequencing of mice with Helicobacter pylori infection and/or KRAS-driven metaplasia

Project description:Stomachs from mice +/- H. pylori infection, +/- induction of active KRAS in gastric Mist1-expressing cells, were used for gastric single-cell RNA-sequencing. Samples were obtained six and 12 weeks after infection/KRAS induction. Six samples were frozen, then thawed before sequencing (and in some cases pooled from multiple mice) and two samples were freshly prepared and never frozen before sequencing.

2023-02-11 | GSE224840 | GEO

Expression data from 6-month Helicobacter felis-infected WT and Gli1-/- mouse stomachs

Project description:Gli1 is necessary for the progression from chronic gastric inflammation to metaplasia in the stomach. We therefore compared the expression patterns between 6-month H. felis infected WT and Gli1-/- stomachs. Pooled tissue from the gastric fundi of 3 mice per group. Groups are WT, WT + H. felis (6 months), Gli1-/-, and Gli1-/- +H. felis (6 months). All the infected and control mice were obtained from the same experiment.

2013-01-24 | E-GEOD-43693 | biostudies-arrayexpress

Helicobacter pylori

Project description:Genomic characterization of Helicobacter pylori isolates from stomachs of Mice eight weeks post-infection

| PRJDB9272 | ENA

Identification of pathogenic microRNAs in Helicobacter pylori-associated gastric cancer

Project description:To identify dysregulated miRNA(s) upon infection with H. pylori during different pre-malignant and malignant stages of gastric cancer in a mouse model miRNA expression in pre-neoplastic and neoplastic lesions in murine stomachs induced by H. pylori and N-methyl-N-nitrosourea (MNU) after 12 months was profiled by miRNA expression array.

2015-03-04 | E-GEOD-62503 | biostudies-arrayexpress

Helicobacter pylori

Project description:Genomic characterization of Helicobacter pylori isolates from stomachs of Mongolian gerbils eight weeks post-infection

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Role of Mincle overexpression in pneumococcal pneumonia

Project description:Macrophage-inducible C-type lectin (Mincle) dependent sensing of pathogens trig-gers proinflammatory immune responses in professional phagocytes that contribute to protect the host against pathogen invasion. Here, we examined whether overex-pression of Mincle designed to improve early pathogen sensing by professional phagocytes would improve lung protective immunity against Streptococcus pneu-moniae in mice. Proteomic profiling of alveolar macrophages (AM) of Mincle trans-genic (tg) mice stimulated with the Mincle-specific pneumococcal ligand glucosyl-diacylglycerol (Glc-DAG) revealed increased Nlrp3 inflammasome activation and downstream IL-1 cytokine release that was not observed in Glc-DAG stimulated Mincle KO or Nlrp3 KO macrophages. Along this line, Mincle tg mice also responded with a stronger Nlrp3 expression and early proinflammatory cytokine release after challenge with S. pneumoniae, ultimately leading to fatal pneumonia in the Mincle tg mice. Importantly, Nlrp3 inhibitor treatment of Mincle tg mice significantly mitigated the observed hyperinflammatory response to pneumococcal challenge. Together, we show that overexpression of the pattern recognition receptor Mincle triggers in-creased Glc-DAG dependent Nlrp3 inflammasome activation in professional phago-cytes leading to fatal pneumococcal pneumonia in mice, which is amenable to Nlrp3 inhibitor treatment. These data show that ectopic expression of Mincle receptor con-fers increased susceptibility rather than resistance to S. pneumoniae in mice, thus highlighting the importance of an inducible Mincle receptor expression in response to microbial challenge.

2020-10-05 | PXD018752 | Pride

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