STANDARD_NAME WUNDER_INFLAMMATORY_RESPONSE_AND_CHOLESTEROL_UP SYSTEMATIC_NAME M1887 COLLECTION C2:CGP MSIGDB_URL https://www.gsea-msigdb.org/gsea/msigdb/human/geneset/WUNDER_INFLAMMATORY_RESPONSE_AND_CHOLESTEROL_UP NAMESPACE MOUSE_SEQ_ACCESSION DESCRIPTION_BRIEF Genes up-regulated in gastric mucosal tissue of mice on 2% cholesterol [PubChem=5997] diet and infected with H. pylori vs those infected with H. pylori while on 0% cholesterol diet. DESCRIPTION_FULL Helicobacter pylori infection causes gastric pathology such as ulcer and carcinoma. Because H. pylori is auxotrophic for cholesterol, we have explored the assimilation of cholesterol by H. pylori in infection. Here we show that H. pylori follows a cholesterol gradient and extracts the lipid from plasma membranes of epithelial cells for subsequent glucosylation. Excessive cholesterol promotes phagocytosis of H. pylori by antigen-presenting cells, such as macrophages and dendritic cells, and enhances antigen-specific T cell responses. A cholesterol-rich diet during bacterial challenge leads to T cell-dependent reduction of the H. pylori burden in the stomach. Intrinsic alpha-glucosylation of cholesterol abrogates phagocytosis of H. pylori and subsequent T cell activation. We identify the gene hp0421 as encoding the enzyme cholesterol-alpha-glucosyltransferase responsible for cholesterol glucosylation. Generation of knockout mutants lacking hp0421 corroborates the importance of cholesteryl glucosides for escaping phagocytosis, T cell activation and bacterial clearance in vivo. Thus, we propose a mechanism regulating the host-pathogen interaction whereby glucosylation of a lipid tips the scales towards immune evasion or response. PMID 16951684 GEOID GSE3878 AUTHORS Wunder C,Churin Y,Winau F,Warnecke D,Vieth M,Lindner B,Zähringer U,Mollenkopf HJ,Heinz E,Meyer TF CONTRIBUTOR Jessica Robertson CONTRIBUTOR_ORG MSigDB Team EXACT_SOURCE Table 1S FILTERED_BY_SIMILARITY EXTERNAL_NAMES_FOR_SIMILAR_TERMS EXTERNAL_DETAILS_URL SOURCE_MEMBERS AA986709,AF027131,AF050157,AF139242,AF251276,AF263458,AF288694,AI196437,AI256549,AI451537,AI573392,AK019873,AV062588,AV063125,AV064900,AV066595,AV067517,AV068350,AV068688,AV072576,AV073517,AV074170,AV079235,AV080712,AV368858,AV369322,AV372409,AV373095,AV373159,AV373244,AW108522,AW120709,AW494821,BB071992,BB072361,BB072553,BB500383,BE691042,BE948047,BE986076,D87910,L20315,M12376,M15593,M16360,M17962,M18837,M27034,M27134,M27347,M29881,M33151,M33225,M34962,M57696,NM_007443,NM_007611,NM_007769,NM_007848,NM_008194,NM_008199,NM_008470,NM_008620,NM_009141,NM_009196,NM_009244,NM_009283,NM_009477,NM_009705,NM_009735,NM_009787,NM_009807,NM_009841,NM_009896,NM_009982,NM_010257,NM_010260,NM_010380,NM_010382,NM_010386,NM_010387,NM_010388,NM_010390,NM_010392,NM_010394,NM_010395,NM_010398,NM_010399,NM_010639,NM_010724,NM_010915,NM_011530,NM_011575,NM_011579,NM_011638,NM_011645,NM_011905,NM_013585,NM_013640,NM_013653,NM_013825,NM_015774,NM_016917,NM_019467,NM_020557,NM_021281,NM_021443,NM_025583,NM_207105,U03064,U03065,U03066,U03067,U12559,U19315,U47328,U69488,X00472,X05430,X57349 GENE_SYMBOLS UGT2B28,MUC17,HLA-DQA1,,SERPINI2,PLAC8,UBA7,,,NFKBIZ,,SP110,,,DEFA1,,,,,,,,,,,,,,,,GATM,BST2,NFKBIZ,,,,,IFI44,FLOT1,DUSP28,PSME2,MPEG1,,,,KLK1,,,,CELA1,,,,,LYN,AMBP,CASP7,DMBT1,DEFA5,GK,,KRT16,GBP6,CXCL6,SLC16A1,SERPINA1,STAT1,UPP1,ARG2,B2M,PDIA4,CASP1,CD14,SOCS1,CTSC,GAST,GBP2,HLA-B,HLA-DRB5,HLA-DMA,HLA-DMB,HLA-DMB,HLA-B,HLA-A,,,HLA-E,,KLK1,PSMB8,KLK1,TAP2,TFF3,,TFRC,,TLR2,PSMB9,PSMB10,CCL5,LY75,ERO1A,SLC40A1,AIF1,CMPK2,CTSS,CCL8,CTRB2,HLA-DQB1,,,,,DEFA5,,HLA-A,,KLK1,CD74,TFRC FOUNDER_NAMES