ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR237/DRR237241/DRR237241_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR237/DRR237238/DRR237238_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR237/DRR237236/DRR237236_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR237/DRR237235/DRR237235_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR237/DRR237239/DRR237239_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR237/DRR237238/DRR237238_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR237/DRR237241/DRR237241_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR237/DRR237233/DRR237233_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR237/DRR237236/DRR237236_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR237/DRR237237/DRR237237_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR237/DRR237240/DRR237240_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR237/DRR237234/DRR237234_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR237/DRR237237/DRR237237_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR237/DRR237240/DRR237240_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR237/DRR237235/DRR237235_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR237/DRR237239/DRR237239_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR237/DRR237233/DRR237233_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR237/DRR237234/DRR237234_1.fastq.gzprimaryOK200GenomicsResearch Institute for Microbial Diseaseshttps://www.ebi.ac.uk/ena/browser/view/PRJDB10162mouse metagenomeHelicobacter pylori (H. pylori) causes assorted gastrointestinal disorders. H. pylori-specific T cells develop during infection, which is 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 a-glucoside (aCAG) 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.ENAMetagenomes, Mus musculus, determination, Laboratory, Swiss, mice, Mus domesticus, mouse, Swiss Mouse, House Mice, Swiss Mice, House Mouse, domesticus, Laboratory Mice, anterior intestine, Stomachs, House, Mus, stomach chamber, chemical analysis, Mus musculus domesticus, Mouse, mesenteron, assay, house mouse, ventriculus., gaster, Mice, Laboratory MouseMus musculus, Metagenomes., House, Mus, Laboratory, Swiss, mice, Mus domesticus, mouse, Mus musculus domesticus, Swiss Mouse, Mouse, House Mice, Swiss Mice, house mouse, Mice, Laboratory Mouse, House Mouse, domesticus, Laboratory Micefalsemouse metagenomeAnalysis of metagenome collected from H. pylori-infected mouse stomach2023-05-192020-09-26PRJDB101621441287