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

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

PROVIDER: PRJNA963900 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24358438_1.fastq.gz	Fastqsanger.gz
	SRR24358438_2.fastq.gz	Fastqsanger.gz
	SRR24358439_1.fastq.gz	Fastqsanger.gz
	SRR24358439_2.fastq.gz	Fastqsanger.gz
	SRR24358440_1.fastq.gz	Fastqsanger.gz

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

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

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

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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.

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Project description:We are investigating the mRNA expression profiles of gastric tissue within H. pylori-infected mice treated with estradiol, tamoxifen, or placebo We used microarrays to compare the global mRNA expression profiles in H. pylori infected mice in response to estradiol and tamoxifen Male mice were infected with H. pylori. After 16 weeks of H.pylori infection, mice were treated with 17beta-estradiol, Tamoxifen or placebo pellets implated subcutaneously for 12 weeks. At that point, longitudinal strips of gastric tissue were snap-frozen. Tissue was later weighed and RNA extracted using Trizol and purified with RNeasy kit including DNase treatment. 9 samples with 3 groups (n= 3 per group, except Tamoxifen (n=2)). Placebo samples are controls and were compared to estradiol or Tamoxifen treated samples.

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Project description:Helicobacter pylori (H. pylori) is a type of pathogen in humans that has infected nearly half of the population worldwide. Infections with H. pylori are typically associated with chronic gastritis and may even lead to gastric and duodenal ulcers and stomach cancer. While the mechanisms behind persistent colonization by H. pylori and the development of gastritis associated with it remain unclear, it is generally believed that the gastric epithelial cells (GECs) modulated by H. pylori in the gastric mucosa play a crucial role. We extensively studied the global gene expression patterns in H. pylori-infected AGS cells, a line of gastric epithelial cells, and identified genes that show increased expression upon infection with H. pylori.

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